bims-mikwok Biomed News
on Mitochondrial quality control
Issue of 2026–05–17
68 papers selected by
Gavin McStay, Liverpool John Moores University



  1. Front Endocrinol (Lausanne). 2026 ;17 1793182
      [This corrects the article DOI: 10.3389/fendo.2023.1160155.].
    Keywords:  diabetic retinopathy; mitochondria; mitochondrial dynamics; mitofusin; mitophagy; retina
    DOI:  https://doi.org/10.3389/fendo.2026.1793182
  2. Bioessays. 2026 May;48(5): e70146
      Mitochondria are vital not only for energy production but also for regulating signaling pathways that influence aging. While mitochondrial dysfunction contributes to age-related decline, emerging evidence shows that mild, regulated mitochondrial stress can paradoxically promote longevity. This review highlights recent advances in mitochondrial biology and aging across species. We explore the dual role of reactive oxygen species (ROS) as both damaging agents and signaling molecules that activate adaptive stress responses. Key pathways such as the mitochondrial unfolded protein response (UPRMT) and integrated stress response (ISR) are discussed, including their tissue-specific as well as non-cell-autonomous effects on aging. Additionally, we examine the impact of mitochondrial protein import/export, dynamics (fission, fusion, mitophagy, biogenesis), and quality control in aging. Finally, we address challenges in understanding context-dependent mitochondrial responses and mitonuclear communication. Together, these insights position mitochondria as central regulators of aging and highlight their potential as therapeutic targets to enhance health span and longevity.
    Keywords:  aging; integrated stress response; mitochondria ROS; mitochondrial dynamics; mitochondrial unfolded protein response
    DOI:  https://doi.org/10.1002/bies.70146
  3. Mol Neurobiol. 2026 May 15. pii: 630. [Epub ahead of print]63(1):
      Cerebral ischemia-reperfusion injury (CIRI) refers to a cascade of pathological events initiated by the restoration of blood flow to ischemic brain regions in patients with cerebral infarction. This process leads to mitochondrial dysfunction through mechanisms including oxidative stress, calcium overload, inflammation, and impaired energy metabolism. FUN14 domain containing 1 (FUNDC1), a key receptor protein involved in mitochondrial autophagy, plays a crucial protective role in CIRI by regulating mitophagy and maintaining mitochondrial quality control. This function is governed by the dynamic phosphorylation and dephosphorylation of FUNDC1, which finely modulate the activation and inhibition of mitophagy, thereby attenuating mitochondrial dysfunction. Moreover, FUNDC1 is implicated in mitochondrial fission, the clearance of unfolded proteins, mitochondrial iron metabolism, and inter-organelle communication, collectively contributing to the regulation of cellular metabolism and immune responses. Therefore, targeting FUNDC1-mediated mitophagy to restore mitochondrial quality control and reduce mitochondrial dysfunction represents a promising therapeutic strategy for CIRI. This review summarizes the role of FUNDC1 in mitochondrial dynamic homeostasis, inter-organelle communication, and CIRI, highlighting its potential as a therapeutic target.
    Keywords:  Cerebral ischemia-reperfusion injury; FUNDC1; Mitochondrial autophagy; Mitochondrial dysfunction; Receptor protein
    DOI:  https://doi.org/10.1007/s12035-026-05923-8
  4. J Ethnopharmacol. 2026 May 08. pii: S0378-8741(26)00699-9. [Epub ahead of print]368 121847
       ETHNOPHARMACOLOGICAL RELEVANCE: Pholidota chinensis Lindl. (P. chinensis), a traditional medicinal plant, exhibits notable antioxidant, anti-inflammatory, and antidiabetic properties. In Traditional Chinese Medicine, its pseudobulbs are applied for treating cough, bronchitis, diabetes, and diabetic kidney disease (DKD). The potential mechanism through which P. chinensis alleviates DKD requires further investigation.
    AIM OF THE STUDY: This investigation was designed to evaluate the potential of P. chinensis to optimize mitochondrial function via the dual regulation of dynamic remodeling and mitophagic flux within DKD models.
    MATERIALS AND METHODS: A DKD animal model was induced through unilateral nephrectomy and streptozotocin administration. Various parameters were evaluated, such as renal function, histopathology, inflammatory and fibrotic markers, and proteins related to mitochondrial fission-fusion balance and mitophagy. In vitro, AGEs-treated HK-2 cell model was employed to assess autophagic flux and mitochondrial function via adenoviral mCherry-GFP-LC3B transduction, JC-1 assay, together with measurements of ROS and ATP production.
    RESULTS: P. chinensis showed clear renoprotective effects in DKD rats, mainly by alleviating renal inflammation and fibrotic changes. Treatment was associated with improved mitochondrial dynamics, characterized by increased expression of mitochondrial fusion-related proteins (Mfn1, Opa1) and reduced levels of fission-related proteins (Drp1, Fis1). Meanwhile, a pronounced activation of mitophagy was observed, evidenced by increased levels of core regulators involved in the PINK1/Parkin pathway and autophagosome formation, along with reduced p62 accumulation. In vitro, P. chinensis exerted antioxidative effects by enhancing SOD activity while reducing MDA levels. It also facilitated autophagy activation and autophagosome-lysosome fusion, leading to improved mitochondrial membrane potential, reduced ROS production, and increased ATP generation.
    CONCLUSION: Overall, P. chinensis improves mitochondrial quality control by promoting fusion, reactivating mitophagy, and enhancing autophagic flux, thereby facilitating mitochondrial clearance and contributing to the attenuation of kidney injury and the slowing of DKD progression.
    Keywords:  Diabetic kidney disease; Inflammation; Kidney fibrosis; Mitochondrial fission–fusion balance; Mitophagy; Pholidota chinensis Lindl
    DOI:  https://doi.org/10.1016/j.jep.2026.121847
  5. Trends Cell Biol. 2026 May 12. pii: S0962-8924(26)00066-8. [Epub ahead of print]
      The AMP-activated protein kinase (AMPK) may have arisen soon after the endosymbiosis event that generated eukaryotes, perhaps to allow the archaeal host to communicate its requirements for ATP to the bacterial endosymbionts that became mitochondria. Consistent with this, AMPK is now known to regulate most aspects of the mitochondrial life cycle. It drives fragmentation of the network by promoting fission and inhibiting fusion, increasing mitochondrial number while allowing isolation of dysfunctional fragments from the network. It promotes the biogenesis of new mitochondrial components while also regulating mitophagy, promoting the degradation of dysfunctional mitochondria and inhibiting the removal of functional mitochondria. We will discuss these new findings and propose that the regulation of mitochondria was an ancient function of AMPK originating in the early eukaryote.
    Keywords:  endosymbiosis; mitochondrial biogenesis; mitochondrial fission; mitochondrial fusion; mitophagy; origin of eukaryotes
    DOI:  https://doi.org/10.1016/j.tcb.2026.04.008
  6. Eur J Pharmacol. 2026 May 13. pii: S0014-2999(26)00457-7. [Epub ahead of print] 178975
      Mitochondrial dysfunction in the retinal pigment epithelium (RPE) is a key pathological feature of age-related macular degeneration (AMD). However, mechanistically defined experimental models that recapitulate stress-mediated mitochondrial injury remain limited. Bcl-2-associated X (BAX), a key pro-apoptotic effector, serves as a critical upstream regulator of mitochondrial outer membrane permeabilization. In this study, we systematically characterized mitochondrial dysfunction induced by BAX trigger site activator 1 (BTSA1), a selective small-molecule BAX activator, in ARPE-19 cells. Treatment with BTSA1 (3-60 μM) for 24 and 48 h induced a concentration- and time-dependent reduction in cell viability, accompanied by caspase-3 activation. Mitochondrial membrane potential, assessed via tetramethylrhodamine ethyl ester staining, was markedly reduced in a BAX-dependent manner and associated with increased reactive oxygen species production following prolonged exposure or at high concentrations. BTSA1 profoundly altered mitochondrial dynamics by promoting DRP1-mediated fission while suppressing fusion through MFN2 downregulation and stress-associated OPA1 processing, resulting in pronounced mitochondrial fragmentation. Furthermore, BAX activation elicited a biphasic response in mitochondrial quality control pathways: mild stress induced impaired autophagic flux and compensatory mitochondrial biogenesis, whereas severe stress triggered mitophagy accompanied by failure of biogenic compensation. These coordinated alterations closely mirror mitochondrial pathologies observed in the degenerating RPE in AMD. Collectively, our findings demonstrate that BAX activation by BTSA1 is sufficient to induce a comprehensive cascade of mitochondrial dysfunction. This system represents a mechanistically defined experimental model for dissecting BAX-mediated mitochondrial pathology and evaluating therapeutic strategies to preserve mitochondrial integrity in AMD.
    Keywords:  Age-related macular degeneration (AMD); BAX activation; Mitochondrial dynamics; Mitochondrial dysfunction; Mitochondrial quality control; Retinal pigment epithelium (RPE)
    DOI:  https://doi.org/10.1016/j.ejphar.2026.178975
  7. Cell Physiol Biochem. 2026 May 11. 60(3): 260-269
       BACKGROUND/AIMS: The Toll-like receptor 4 (TLR4) pathway plays a critical role in mediating inflammatory responses and regulates mitochondrial structural adaptations. Urolithin A (UA), a natural compound that induces mito- and autophagy, may improve mitochondrial homeostasis and health. This study examined the effects of UA on TLR4 signaling, mitochondrial dynamics, autophagy, and mitochondrial morphology after lipopolysaccharide (LPS) incubation in C2C12 myotubes.
    METHODS: C2C12 myotubes were incubated with LPS (1 µg/ml) and/or UA (50 µM). Protein expression related to TLR4 signaling, mitochondrial dynamics, and autophagy was assessed by Western blot, while mitochondrial morphology was evaluated using electron microscopy.
    RESULTS: LPS-induced inflammation activated downstream TLR4 signaling pathways and altered mitochondrial morphology, including reduced mitochondrial area and circularity. LPS also increased phosphorylation of the mitochondrial fission marker DRP1. UA prevented or attenuated these alterations induced by LPS.
    CONCLUSION: UA partially mitigates LPS-induced inflammation through modulation of TLR4 signaling and mitochondrial dynamics and may represent a promising therapeutic strategy for disorders associated with mitochondrial dysfunction and inflammation.
    Keywords:  TLR4 ; Inflammation ; Urolithin A ; Mitochondrial homeostasis ; Myotubes
    DOI:  https://doi.org/10.33594/000000869
  8. Stem Cell Res Ther. 2026 May 09.
       BACKGROUND: Intervertebral disc degeneration (IVDD) is a major cause of low back pain, characterized by mitochondrial dysfunction and impaired mitophagy in nucleus pulposus-derived mesenchymal stem cells (NPMSCs). Sirtuin 1 (SIRT1), a key regulator of mitochondrial quality control, is downregulated in degenerated discs. Salidroside (Sal), a natural compound from Rhodiola rosea, has shown potential in enhancing mitophagy, but its mechanism in IVDD remains unclear.
    METHODS: Using network pharmacology, molecular docking, and dynamics simulations, we identified SIRT1 as a key target of Sal. Human and rat NPMSCs were isolated and treated with tert-butyl hydroperoxide (TBHP) to induce degeneration. In vitro assays included CCK-8, EdU, SA-β-Gal, JC-1, Western blot, immunofluorescence, and transmission electron microscope (TEM). An in vivo rat IVDD model was established via needle puncture and treated with Sal and/or the autophagy inhibitor 3-MA. Histological, immunohistochemical, and imaging analyses were performed to evaluate IVDD.
    RESULTS: Sal bound stably to SIRT1 and activated SIRT1/FOXO3 pathway, promoting mitophagic flux, reducing reactive oxygen species accumulation, and suppressing apoptosis in NPMSCs. SIRT1 knockdown or 3-MA treatment abolished Sal's protective effects. In vivo, Sal treatment preserved disc height, reduced apoptosis, and enhanced mitophagy, while 3-MA exacerbated degeneration.
    CONCLUSIONS: Sal attenuates IVDD by activating SIRT1/FOXO3-mediated mitophagy, restoring mitochondrial homeostasis, and reducing NPMSCs apoptosis. These results suggest that the activation of the SIRT1/FOXO3-mitophagy axis may represent a potential therapeutic strategy for mitigating IVDD.
    Keywords:  Apoptosis; Mitophagy; Nucleus pulposus-derived mesenchymal stem cells; SIRT1/FOXO3; Salidroside
    DOI:  https://doi.org/10.1186/s13287-026-05051-z
  9. Int J Mol Sci. 2026 Apr 25. pii: 3828. [Epub ahead of print]27(9):
      Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation, epithelial barrier disruption and immune dysfunction. Alleviating and curing these pathological manifestations is the goal of IBD treatment. Despite substantial advances in targeted immunotherapies and anti-inflammatory strategies, achieving sustained intestinal mucosal healing remains a major clinical challenge. Dynamin-related protein 1 (Drp1) is a GTPase that mediates mitochondrial fission and plays a crucial role in maintaining the dynamic balance of mitochondrial morphology and function. In IBD, Drp1 expression is frequently upregulated and continuously activated, resulting in excessive fission and fragmentation of mitochondria. This mitochondrial dysregulation contributes to ATP depletion and excessive reactive oxygen species (ROS) production, thereby exacerbating disease progression and amplifying inflammatory signaling. This review highlights the distinctive role of Drp1 as an integrative node in IBD. Specifically, we connect mitochondrial dynamics with epithelial barrier failure, immune dysregulation, inflammatory cell death, and intestinal microenvironment remodeling. We further emphasize the potential relevance of Drp1 for biomarker-based patient stratification and mechanism-informed therapeutic targeting, thereby distinguishing this review from more descriptive accounts of mitochondrial dysfunction in intestinal inflammation.
    Keywords:  dynamin-related protein 1; inflammation; inflammatory bowel disease; intestinal epithelial barrier; mitochondrial dynamics; mitochondrial fission
    DOI:  https://doi.org/10.3390/ijms27093828
  10. Aging Cell. 2026 May;25(5): e70539
      Aging is a major risk factor for numerous diseases, including degenerative and metabolic disorders. Cumulative mitochondrial damage, elevated reactive oxygen species (ROS), and impaired mitophagy are hallmarks of aging. In this study, we generated a Drosophila version of the mito-SRAI reporter to monitor mitophagy in vivo and demonstrated an age-dependent decline in muscle mitophagy, accompanied by the accumulation of insoluble proteins, increased ROS levels, and mitochondrial damage. Overexpression of BNIP3 preserved muscle homeostasis by enhancing mitophagy, maintaining mitochondrial integrity, and suppressing ROS accumulation. Importantly, muscle-specific expression of BNIP3 in indirect flight muscles extended lifespan and alleviated age-associated neurodegenerative phenotypes, including protein aggregation, β-galactosidase accumulation, and pathological vacuolization in the brain. Mechanistically, BNIP3 inhibited ROS-mediated activation of Relish, thereby reducing expression of antimicrobial peptide (AMP) genes. These findings identify BNIP3 as a key regulator of aging that links mitochondrial quality control to systemic aging and neurodegeneration. Moreover, our results provide direct evidence of muscle-to-brain signaling, revealing a non-autonomous mechanism by which muscle mitophagy mitigates age-related neurodegeneration.
    Keywords:  BNIP3; aging; inflammation; mitophagy; neurodegeneration; non‐autonomous regulation
    DOI:  https://doi.org/10.1111/acel.70539
  11. FASEB J. 2026 May 31. 40(10): e71812
      The Integrated Stress Response (ISR) is a vital cellular mechanism that regulates cell survival during various stress conditions, including hypoxia. Activating transcription factor 4 (ATF4) is recognized as a key regulator of ISR, however, its role in hypoxic stress responses remain underexplored. In the present study, we generated an Atf4a-deficient zebrafish model to investigate the role of Atf4a in hypoxia tolerance, mitochondrial homeostasis, and cellular stress adaptation. The results showed that atf4a knockout led to significant growth impairment, endoplasmic reticulum and mitochondrial dysfunction, and disrupted energy metabolism, particularly under hypoxic conditions. We observed an increase in mitochondrial DNA and impaired mitochondrial morphology in Atf4a-deficient zebrafish. Metabolomic analysis revealed significant alterations in the pentose phosphate pathway and TCA cycle following atf4a knockout. Additionally, we observed increased mitochondrial oxidative stress and reduced antioxidant capacity in atf4a mutants. Atf4a-deficiency also led to decreased expression of the mitophagy-related gene p62 and parkin. Atf4a transcriptionally regulates the expression of parkin, suggesting that Atf4a regulates mitochondrial homeostasis through parkin-mediated mitophagy in zebrafish. These results underscore the critical role of Atf4a in maintaining cellular homeostasis, mitochondrial integrity, and metabolic adaptation during hypoxic stress, highlighting its potential as a therapeutic target for stress-related diseases.
    Keywords:  ATF4; ISR; hypoxia; mitophagy; parkin
    DOI:  https://doi.org/10.1096/fj.202502855R
  12. Mitochondrion. 2026 May 14. pii: S1567-7249(26)00052-8. [Epub ahead of print] 102162
      Mitochondrial dynamics, regulated by the balance of fission and fusion, are essential for cellular homeostasis, and their disruption-particularly via excessive Drp1-dependent fission-contributes to cancer and other pathologies. Current Drp1 inhibitors lack specificity or exhibit off-target toxicity, highlighting the need for safer alternatives. Here, we identify FRAG-i, a small-molecule Drp1 inhibitor discovered through multi-stage virtual screening and molecular dynamics refinement of a 3.5-million-compound library. FRAG-i binds the Drp1 GTPase domain with high affinity (Kd = 732.4 ± 4.2 nM) and increases Drp1 thermal stability in recombinant and cellular assays. Functionally, FRAG-i selectively suppresses mitochondrial fission in A549 lung carcinoma cells while sparing the fused networks of non-cancerous BEAS-2B epithelial cells. FRAG-i preserves mitochondrial membrane potential, ATP levels, and redox balance without cytotoxicity, and modulates Drp1, MiD49, and Mfn2 expression in a context-dependent manner. These results establish FRAG-i as a selective, non-toxic Drp1 inhibitor with potential for further therapeutic development.
    Keywords:  Drp1; Fission; Mitochondrial dynamics; Small molecule inhibitors
    DOI:  https://doi.org/10.1016/j.mito.2026.102162
  13. Am J Physiol Cell Physiol. 2026 May 13.
      Protein homeostasis is critical for mitochondrial function and is maintained by proteases and chaperones that respond to stress and mediate adaptive changes such as the mitochondrial unfolded protein response (UPRmt), the integrated stress response (ISR) and antioxidant signaling. However, the mechanisms by which stressors regulate these retrograde responses remains uncharacterized in muscle. Thus, we examined the effect of mitochondrial stressors on the activation of these pathways in myoblasts and differentiated myotubes. Cells were exposed to either 1) CDDO, a LonP1 protease inhibitor, 2) GTPP, an HSP90 chaperone inhibitor, 3) CCCP, an energetic uncoupler, or 4) MB-10, an inhibitor of protein import, and responses were compared to those induced by acute contractile activity (ACA). LonP1 inhibition activated ATF4 and Nrf2 signaling, increased mitochondrial chaperones, and resulted in protein aggregation without elevating reactive oxygen species (ROS). In contrast, blocking HSP90 led to increases in mitochondrial ROS and activation of CHOP, indicating protein homeostasis-related stress with limited antioxidant signaling. ACA elicited responses similar to the inhibition of LonP1, including the activation of ATF4 and Nrf2, increased UPRmt markers, and a redox balance. Although CCCP and MB-10 both impaired protein import, they activated distinct downstream responses. CCCP resulted in ISR activation, while MB-10 induced Nrf2-mediated antioxidant responses. Together, these findings show that the type of mitochondrial stress determines the direction of the retrograde signaling pathways between protein homeostasis and redox signaling in muscle cells, and they provide insights on how muscle coordinates signaling pathways as part of mitochondrial adaptations to contractile activity.
    Keywords:  integrated stress response; mitochondrial biogenesis; mitochondrial proteostasis; mitochondrial unfolded protein response; muscle contractile activity
    DOI:  https://doi.org/10.1152/ajpcell.00167.2026
  14. J Cell Biol. 2026 Jun 01. pii: e202603198. [Epub ahead of print]225(6):
      Mitochondrial dynamics regulate mitochondrial activity through several pathways, but their coordination remains unclear. Zhao et al. (https://doi.org/10.1083/jcb.202508040) show that endosomal PI(3)P promotes CDC42-dependent actin polymerization on mitochondria, providing insight into the upstream signals regulating mitochondrial dynamics.
    DOI:  https://doi.org/10.1083/jcb.202603198
  15. Front Cell Dev Biol. 2026 ;14 1813085
      Endometriosis (EMs) is a gynecological disorder affecting women of reproductive age. It is characterized by the ectopic implantation and infiltration of endometrial-like tissue and is associated with significant effects on fertility, pelvic function, and overall wellbeing. Clinically, it presents with progressive secondary dysmenorrhea, chronic pelvic pain, and infertility, leading to a substantial reduction in quality of life. Despite decades of research, the pathogenesis of EMs remains complex and is driven by interacting hormonal, immunological, inflammatory, and metabolic factors. Current treatment approaches, including hormonal suppression and surgical excision, provide only temporary relief and are associated with systemic side effects, functional limitations, and high recurrence rates. These limitations highlight the need for safer and more effective therapeutic strategies. Mitochondria play a central role in the development of EMs. Mitochondrial function is regulated by the mitochondrial quality control (MQC) system, which consists of several interconnected processes, including redox homeostasis, mitochondrial fission and fusion, mitophagy, biogenesis, and calcium signaling. Increasing evidence suggests that disruption of MQC is not merely a secondary effect but a key contributor to EMs pathogenesis. MQC dysfunction enables ectopic endometrial cells to evade apoptosis, promotes invasive proliferation, supports oxidative stress adaptation, and facilitates survival in unfavorable microenvironments. Plant-derived compounds have gained attention as potential modulators of MQC. These compounds exhibit multi-target effects, favorable safety profiles, and a wide range of bioactive structures. Experimental studies indicate that botanical agents, including flavonoids and terpenoids, can regulate multiple components of the MQC system. They reduce mitochondrial reactive oxygen species, modulate DRP1/OPA1-mediated mitochondrial dynamics, enhance PINK1-Parkin-dependent mitophagy, promote PGC-1α-mediated mitochondrial biogenesis, and maintain calcium homeostasis. Through these mechanisms, phytochemicals improve mitochondrial function, inhibit abnormal cell survival signaling, induce apoptosis in ectopic lesions, and contribute to the restoration of endometrial homeostasis.
    Keywords:  endometriosis; mitochondrial quality control system; phytomedicine; plant active ingredients; regulatory mechanism
    DOI:  https://doi.org/10.3389/fcell.2026.1813085
  16. Kidney Res Clin Pract. 2026 May 11.
      Diabetic kidney disease (DKD) is a leading cause of end-stage renal disease worldwide, affecting over 40% of individuals with diabetes. Despite advances in glycemic control and renin-angiotensin system blockade, effective therapeutic strategies remain limited. A narrative review was synthesized from research papers using PubMed, Wiley Online Library, ScienceDirect, Cochrane Library, Springer, and other sources, published between 2000 and 2025 with logical combinations of appropriate keywords and Medical Subject Headings. Emerging evidence implicates mitochondrial dysfunction as the central pathogenic mechanism underlying DKD progression. Mitochondria govern critical cellular processes, comprising energy metabolism, reactive oxygen species homeostasis, and cell survival. In DKD, hyperglycemia-induced metabolic stress compromises mitochondrial oxidative phosphorylation, enhances reactive oxygen species production, damages mitochondrial DNA, as well as disrupts mitochondrial dynamics through aberrant fission, fusion, and mitophagy processes. These alterations occur early in the pathogenesis of disease and affect multiple renal cell types, particularly proximal tubular epithelial cells and podocytes. Recent studies have identified key molecular regulators of mitochondrial quality control, including PTEN-induced putative kinase 1/Parkin-mediated mitophagy, dynamin-related protein 1-driven fission, and peroxisome proliferator-activated receptor gamma coactivator 1-αlpha-dependent biogenesis, as potential therapeutic targets. Novel therapies targeting mitochondrial dysfunction, including sodium-glucose cotransporter 2 (SGLT2) inhibitors, mitochondria-targeted antioxidants, and metabolic modulators, have shown promise in preclinical and clinical studies. This paper synthesizes recent understanding of mitochondrial metabolism and dynamics in DKD pathogenesis and evaluates emerging mitochondria-directed therapeutic strategies. This review concludes that only SGLT2 inhibitors are the only class of drugs with robust randomized controlled trial evidence to date and other emerging therapeutic options require further clinical validation.
    Keywords:  Diabetic kidney disease; Mitochondrial dynamics; Mitochondrial dysfunction; Mitophagy; Oxidative phosphorylation; Sodium-glucose transporter 2 inhibitors
    DOI:  https://doi.org/10.23876/j.krcp.25.413
  17. Zhongguo Zhen Jiu. 2026 May 12. 46(5): 743-752
       Objective: To investigate the effect of Xingnao Kaiqiao acupuncture therapy (for regaining the consciousness and opening the orifices) on cerebral mitochondrial dynamics homeostasis in middle cerebral artery occlusion/reperfusion (MCAO/R) model rats, and to explore the mechanism of this therapy on cerebral ischemia-reperfusion injury (CIRI).
    Methods: A total of 64 healthy male SD rats were randomly divided into a sham-operation group, a model group, an acupuncture group, and an inhibitor group, with 16 rats in each group. Except for the sham-operation group, the MCAO/R model was established in the remaining groups using the modified Longa's method. In the acupuncture group, acupuncture was delivered at bilateral "Neiguan" (PC 6) and "Shuigou" (GV 26), for 30 min per intervention, once daily for 5 consecutive days. In the inhibitor group, the mitochondrial division inhibitor 1 (Mdivi-1) was injected intraperitoneally (2 mg/kg), once daily for 5 consecutive days. Separately, before cerebral ischemia, after ischemia, after ischemia-reperfusion and after intervention completion, using a laser speckle contrast imaging (LSCI) system, the cerebral blood perfusion in the affected cerebral cortex region was monitored. After intervention completion, the neurological deficits were evaluated using the Bederson score; the grip strength was measured with a small animal grip meter; the cerebral infarction volume percentage was quantified via 2,3,5-triphenyltetrazolium chloride (TTC) staining; the mitochondrial ultrastructure in endothelial cells within the ischemic penumbra (IP) region of the cerebral cortex was observed using transmission electron microscopy; the fluorescence co-localization area of optic atrophy 1 (OPA1) and the endothelial cell marker CD31 in the cortical IP region was analyzed by immunofluorescence; the protein expression of mitochondrial fusion protein 2 (MFN2), OPA1, and dynamin-related protein 1 (DRP1) in the cortical IP region was detected using Western blot.
    Results: Except in the sham-operation group, cerebral blood perfusion in the affected cerebral cortex decreased after cerebral ischemia in the rest groups compared with that before cerebral ischemia (P<0.001). When compared with the time point after cerebral ischemia, cerebral blood perfusion in the affected cerebral cortex was elevated after cerebral ischemia-reperfusion in each group (P<0.001). After intervention completion, in comparison with the model group, the ratios of cerebral blood perfusion were elevated in both the acupuncture group and the inhibitor group (P<0.001); and the ratio of cerebral blood perfusion rose in the acupuncture group compared with that in the inhibitor group (P<0.001). Compared with the sham-operation group, the model group exhibited the increase of neurological deficit score and cerebral infarction volume percentage (P<0.001), and the decline of grip strength (P<0.001). When compared with the model group, both the acupuncture group and the inhibitor group showed the decrease of neurological deficit scores and cerebral infarction volume percentage (P<0.01, P<0.05, P<0.001), and the increase of grip strength (P<0.001). Compared with the inhibitor group, cerebral infarction volume percentage was lower and grip strength was higher in the acupuncture group (P<0.001). In the model group, the endothelial cell mitochondria exhibited severe swelling, exhibiting a spherical morphology predominantly, with extensive cristae fragmentation or even disappearance, and excessive vacuolization. In both the acupuncture group and the inhibitor group, the ultrastructural damage to endothelial cell mitochondria was partially ameliorated; the acupuncture group demonstrated a superior restoration of mitochondrial ultrastructure in comparison with the inhibitor group. When compared with the sham-operation group, the area ratio of co-localization of OPA1 and CD31 decreased in the model group (P<0.001). The area ratio of co-localization of OPA1 and CD31 increased in either the acupuncture group or the inhibitor group in comparison with the model group, respectively (P<0.001). The area ratio of co-localization of OPA1 and CD31 in the acupuncture group was higher than that of the inhibitor group (P<0.001). Compared with the sham-operation group, the model group exhibited the lower protein expression of MFN2 and OPA1 (P<0.001) and protein higher expression of DRP1 (P<0.001). When compared with the model group, the acupuncture group showed the increase of protein expression of MFN2 and OPA1 and the decrease of DRP1 protein expression (P<0.001, P<0.05), while in the inhibitor group, the protein expression of MFN2 was elevated and that of DRP1 declined (P<0.05, P<0.01). When compared with the inhibitor group, the acupuncture group displayed higher MFN2 expression (P<0.01) and lower DRP1 expression (P<0.01).
    Conclusion: Xingnao Kaiqiao acupuncture therapy mitigates neurological deficits and enhances cerebral blood supply of ischemic region in MCAO/R rats, and the underlying mechanism may be related to regulating mitochondrial dynamics homeostasis of endothelial cells in the IP of cerebral cortex, and attenuating mitochondrial damage.
    Keywords:  Xingnao Kaiqiao acupuncture therapy; cerebral ischemia-reperfusion injury; dynamin-related protein 1 (DRP1); mitochondrial dynamics; mitochondrial fusion protein 2 (MFN2); optic atrophy 1 (OPA1)
    DOI:  https://doi.org/10.13703/j.0255-2930.20241218-k0004
  18. Cells. 2026 Apr 29. pii: 806. [Epub ahead of print]15(9):
      Embryos being treated using assisted reproductive technology (ART) are unavoidably exposed to physical stressors, thus producing reactive oxygen species (ROS) which trigger mitophagy to support embryonic development. However, the mechanisms underlying the regulation of mitophagy in early embryonic development remain largely unexplored. Here, we found that Mucin 1 (MUC1) exhibited a uniform distribution in both mouse and human oocytes, and its expression peaked at the blastocyst stage. Further analysis revealed that Muc1 knockout impairs blastocyst formation in vitro. Correspondingly, Muc1 knockout led to the accumulation of mitochondrial reactive oxygen species (mtROS) and a reduction in phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1)/Parkinson protein 2 (PARK2/Parkin)-dependent mitophagy. Stimulation of mitophagy via low-dose carbonyl cyanide 3-chlorophenylhydrazone (CCCP) treatment rescued the blastocyst formation defect in Muc1-null embryos. Vitamin C supplementation effectively scavenged mtROS and restored developmental competence. Together, our findings establish that MUC1 safeguards early embryonic development by promoting mitophagy to decrease mtROS levels in vitro. Moreover, vitamin C could compensate for Muc1 deficiency by eliminating mtROS. This study not only identified a new function of MUC1 in protecting early embryonic development in vitro, but also revealed a novel mechanism of mitophagy regulation in early embryos, which has potential applications for ART.
    Keywords:  MUC1; ROS; embryos; mitophagy; preimplantation
    DOI:  https://doi.org/10.3390/cells15090806
  19. Biophys Rep. 2026 Apr 30. 12(2): 116-125
      Ferroptosis is a new form of cell death driven by iron-dependent lipid peroxidation. Thus, it is closely related to the lipid and iron metabolism. Accumulating evidence has suggested mitochondria, the center of cell metabolism, are important regulators of ferroptosis. This is not surprising as mitochondria are also the center for lipid metabolism and iron metabolism, as well as redox balance. As the essential way of mitochondrial quality control, mitophagy may alleviate ferroptosis. On the other hand, the digestion of iron-rich mitochondria may provide ample sources for the activation of ferroptosis. This review describes these new findings about the interplay of mitophagy and ferroptosis and demonstrates the dual role of mitophagy in ferroptosis.
    Keywords:  Ferroptosis; Iron; Mitophagy; ROS
    DOI:  https://doi.org/10.52601/bpr.2025.240071
  20. Mater Today Bio. 2026 Jun;38 103173
      Diabetic wound healing remains a formidable clinical challenge. Mitochondrial dysfunction-driven oxidative stress is a central pathological driver of impaired diabetic wound healing, yet targeted interventions for mitochondrial repair and mitophagy modulation are lacking. Herein, we report a mitochondria-targeted selenium-doped carbon dots (Se-CDs) nanozyme hydrogel system (Se-CDs@Gelatin-TA) with potent reactive oxygen species (ROS)-scavenging capacity and PINK1/Parkin-mediated mitophagy-regulating activity for diabetic wound regeneration. The Se-CDs exhibited biocompatibility, broad-spectrum antioxidant activities, specific mitochondrial targeting ability due to selenium doping, and intrinsic blue fluorescence enabled mitochondrial co-localization tracking without external labels. Encapsulation of Se-CDs into a gelatin-tannic acid hydrogel enabled sustained release of the nanozyme. In vitro studies demonstrated that Se-CDs effectively scavenged intracellular and mitochondrial ROS, suppressed high glucose-induced fibroblast apoptosis, and restored mitophagic flux through activation of the PINK1/Parkin pathway an effect abrogated by mitophagy inhibitor 3-MA and siRNA-mediated knockdown of PINK1/Parkin. In vivo, topical application of Se-CDs@Gelatin-TA hydrogel accelerated wound closure, reduced inflammatory infiltration, enhanced collagen deposition, and restored endogenous antioxidant enzyme activity in wound tissues. This work presents a novel nanozyme-based targeted strategy for diabetic wounds, leveraging Se-CDs to modulate mitophagy and redox homeostasis, and provides mechanistic insights into the role of PINK1/Parkin-mediated mitophagy in diabetic wound repair.
    Keywords:  Diabetic wounds; Mitochondrial targeting; PINK1/Parkin mitophagy; Reactive oxygen species; Selenium-carbon dots
    DOI:  https://doi.org/10.1016/j.mtbio.2026.103173
  21. Biochem Pharmacol. 2026 May 09. pii: S0006-2952(26)00373-4. [Epub ahead of print]250(Pt 2): 118040
      Mitochondrial dysfunction and insufficient mitophagy are central to cisplatin-induced acute kidney injury (AKI). Tirzepatide, a dual GLP‑1/GIP receptor agonist, exhibits reno-protective effects, but its mechanism related to mitochondrial homeostasis remains unclear. Here, we used metabolomics, in vivo mouse AKI model, and in vitro cisplatin-injured HK‑2 cells to explore the protective effects and underlying mechanisms. Tirzepatide pretreatment significantly alleviated renal dysfunction, tubular injury, and mitochondrial damage caused by cisplatin. Metabolomic analysis revealed that tirzepatide strongly regulated energy metabolism and autophagy , particularly NAD + homeostasis. Mechanistically, tirzepatide boosted NAD+ levels by nicotinamide phosphoribosyl transferase (NAMPT), the rate-limiting enzyme for NAD + synthesis , which in turn activating the Pink1-Parkin mitophagy pathway. Inhibition of autophagy or NAMPT abolished the mitochondrial and reno-protective effects of tirzepatide. Taken together, our findings demonstrate that tirzepatide protects against cisplatin‑induced AKI by enhancing NAMPT‑dependent NAD + restoration and promoting mitophagy, highlighting a promising therapeutic strategy for chemotherapy‑related nephrotoxicity.
    Keywords:  Autophagy; Mitochondrial homeostasis; NAD+; NAMPT; Tirzepatide
    DOI:  https://doi.org/10.1016/j.bcp.2026.118040
  22. Discov Oncol. 2026 May 09.
       BACKGROUND: Mitophagy plays a vital role in hepatocellular carcinoma (HCC) progression. This study aims to construct a mitophagy-related scoring system and evaluate its prognostic value, association with tumor immune activity, and gene mutation profiles in HCC patients, thereby advancing personalized diagnosis and treatment.
    METHODS: Copy number variation (CNV) data of mitophagy regulators from TCGA and ICGC databases were integrated for consensus clustering. Principal component analysis (PCA) was employed to establish a mitophagy scoring system based on mitophagy clusters, gene clusters, and clinical outcomes. Kaplan-Meier survival analysis, Spearman correlation, and immune infiltration algorithms (CIBERSORT, ssGSEA) were used to assess clinical relevance, prognosis, and immunotherapy sensitivity. Tumor mutation burden (TMB) was combined with mitophagy scores for refined prognosis prediction.
    RESULTS: Three distinct mitophagy clusters (A, B, C) and gene clusters (A, B, C) were identified, showing significant differences in prognosis, immune cell infiltration (19 immune cell types, p < 0.05), and mutation profiles. The mitophagy scoring system stratified patients into high- and low-score groups. High-score patients exhibited better overall survival (p < 0.001), higher immune checkpoint expression (PD-1, CTLA4; p = 0.015 and p = 0.0007), and greater sensitivity to immunotherapy. Low-score patients had higher TP53 mutation rates (55%) and poorer outcomes. Combining mitophagy scores with TMB further improved prognostic accuracy (p < 0.001).
    CONCLUSION: The mitophagy scoring system serves as a robust prognostic biomarker and predictor of immunotherapy response in HCC, offering insights into tumor heterogeneity and clinical decision-making.
    Keywords:  Hepatocellular carcinoma; Immunotherapy; Mitophagy; Prognosis; Tumor mutation burden
    DOI:  https://doi.org/10.1007/s12672-026-05117-7
  23. Mol Biol Cell. 2026 May 13. mbcE25110529
      Hypoxia drives pulmonary artery smooth muscle cells (PASMCs) proliferation and phenotypic remodeling, processes central to vascular adaptation. Yaks, native to high-altitude environments, provide a natural model for studying cellular responses to chronic hypoxia. In this study, hypoxic exposure enhanced yak PASMCs proliferation and induced phenotypic transformation. Transcriptome profiling revealed that hypoxia suppresses microRNA-206 (miR-206), a regulator of vascular smooth muscle homeostasis. Loss of miR-206 activated the HIF-1α/BNIP3-dependent mitophagy pathway, increased mitophagy levels, and accelerated cell-cycle progression. Restoration of miR-206 reversed these effects, confirming its inhibitory role. Mechanistically, miR-206 directly targets the HIF-1α/BNIP3 signaling axis, linking noncoding RNA regulation to mitochondrial quality control under low oxygen. These findings define a miR-206-HIF-1α/BNIP3 regulatory circuit that coordinates mitophagy and phenotypic remodeling in yak PASMCs. This mechanism highlights the contribution of miRNA-mediated mitochondrial regulation to hypoxia adaptation and offers new insight into pulmonary vascular remodeling in high-altitude mammals.
    DOI:  https://doi.org/10.1091/mbc.E25-11-0529
  24. Medicine (Baltimore). 2026 May 08. 105(19): e47600
      Mitophagy, a selective autophagic process responsible for the degradation of dysfunctional mitochondria, serves as a critical regulator of cellular homeostasis. Despite its emerging significance in ocular pathophysiology, comprehensive analyses bridging molecular mechanisms to clinical translation remain scarce. The retina, with its high metabolic demands and reliance on mitochondrial bioenergetics, is particularly vulnerable to mitophagic dysregulation, which has been mechanistically linked to the pathogenesis of major ophthalmic disorders. This review systematically elucidates the molecular architecture of mitophagy, focusing on its dual roles in disease progression and cytoprotection across glaucoma, age-related macular degeneration (AMD), and diabetic retinopathy (DR). By integrating mechanistic insights with therapeutic implications, we not only delineate conserved regulatory pathways (e.g., PINK1 [PTEN-induced kinase 1]/Parkin, BNIP3 [BCL2/adenovirus E1B 19 kDa interacting protein 3], FUNDC1 [FUN14 domain containing 1]) but also propose a roadmap for targeting mitophagic checkpoints through precision pharmacology and combinatorial regimens. Our synthesis underscores the urgency of translating mitophagy modulation into clinical strategies to address unmet needs in retinal degenerative diseases.
    Keywords:  age-related macular degeneration (AMD); diabetic retinopathy (DR); glaucoma; mitophagy; oxidative stress; regulation of autophagy
    DOI:  https://doi.org/10.1097/MD.0000000000047600
  25. Oncogenesis. 2026 May 12.
       ABTRACT: In cancer, mitochondrial fission and fusion dynamics are often imbalanced due to altered transcriptional and post-transcriptional control of their key regulators, resulting in either excessive fission or fusion. Despite being opposing processes, these imbalances in mitochondrial dynamics play a critical role in tumorigenic processes. Excessive fission drives metabolic reprogramming by promoting a shift toward aerobic glycolysis and regulating fatty acid metabolism, whereas excessive fusion supports oxidative phosphorylation and glutaminolysis. Both processes, in their own specific way, enable rapid growth and enhance survival in heterogeneous and unfavorable tumor microenvironments. Beyond metabolic regulation, excessive fission plays a key role in invasion and metastasis by promoting cytoskeletal remodeling for single-cell migration and inducing epithelial-to-mesenchymal transition. Moreover, both excessive fission and fusion can inhibit apoptosis and enhance therapy resistance by modulation of the intrinsic apoptosis pathway, upregulation of antioxidant defenses, and/or activation of autophagy. This review examines how both dysregulated fission and fusion contribute to tumorigenic processes in solid tumors and highlights mitochondrial dynamics as a promising therapeutic target.
    DOI:  https://doi.org/10.1038/s41389-026-00620-6
  26. Autoimmun Rev. 2026 May 07. pii: S1568-9972(26)00086-8. [Epub ahead of print]25(6): 104072
      Systemic lupus erythematosus (SLE) is a persistent autoimmune condition involving multiple organ systems. It is fundamentally driven by the dysregulation of the immune system. Under this condition, the immune system erroneously targets body tissues and induces a marked inflammatory immune response, ultimately leading to multisystem and multi-organ involvement. Mitophagy is a selective intracellular quality control mechanism that eliminates dysfunctional or redundant mitochondria and is crucial for maintaining cellular homeostasis. In recent years, accumulating research has indicated that dysregulated mitophagy is closely linked to the pathogenesis of SLE and associated organ damage, particularly in lupus nephritis (LN). This review systematically elaborates the molecular regulatory network of mitophagy and its specific roles in immune dysregulation and organ damage in SLE. We further explored therapeutic strategies targeting mitophagy to provide new theoretical foundations and directions for the targeted management of SLE.
    Keywords:  Immunity; Mitophagy; Systemic lupus erythematosus; Therapy
    DOI:  https://doi.org/10.1016/j.autrev.2026.104072
  27. FASEB J. 2026 May 31. 40(10): e71886
      Vasorin (VASN), a transmembrane glycoprotein, plays a pivotal role in hepatocellular carcinoma (HCC) progression by regulating cell proliferation and migration. However, its subcellular localization and organelle-specific functional mechanisms remain inadequately defined, mainly due to the limitations of ultrastructural resolution and quantitative analytical techniques. In this study, an optimized immunoelectron microscopy protocol (IEM-VASN) was developed, combining 4% paraformaldehyde-0.5% glutaraldehyde fixation and a 1:200 anti-VASN antibody dilution, achieving an optimal balance between structural preservation and antigenicity. This method enabled the precise detection of VASN depletion in Huh7-KD cells (p < 0.0001) and Vasn-/- mice (p < 0.0001). IEM-VASN revealed VASN's organelle-specific distribution, showing significant enrichment in mitochondria in both HCC cells and liver tissues (p < 0.001 and p < 0.0001). Furthermore, murine HCC tissues displayed elevated VASN levels (p < 0.001) alongside reduced mitochondrial counts (p < 0.01). In a chronic aflatoxin B1 (AFB1) exposure model, VASN upregulation correlated with ROS accumulation, mitochondrial membrane potential dissipation, and mitophagy induction. The IEM-VASN method demonstrated high precision and applicability across cellular, animal, and pathological models, providing a powerful tool for elucidating the functional roles of VASN in HCC. These findings establish a highly sensitive and specific IEM technique for characterizing VASN's ultrastructural distribution, highlighting its predominant mitochondrial localization and functional involvement in HCC progression and chemically-induced mitophagy, thus positioning VASN as a critical molecular mediator in liver cancer and mitochondrial homeostasis.
    Keywords:  aflatoxin B1 (AFB1); hepatocellular carcinoma; immunoelectron microscope; immunogold labeling; mitochondrial autophagy; monoclonal antibody; vasorin (VASN)
    DOI:  https://doi.org/10.1096/fj.202600809R
  28. Mol Biol Rep. 2026 May 11. pii: 742. [Epub ahead of print]53(1):
       BACKGROUND: Migraine is a disabling neurovascular disorder in which neuroinflammation, trigeminal activation, and mitochondrial dysfunction play central roles. Mitochondria-targeted antioxidants such as mitoTEMPO may modulate these mechanisms; however, their effects in nitroglycerin (NTG)-induced migraine models remain unclear. This study investigated the effects of mitoTEMPO on mitochondrial biogenesis, fusion-fission dynamics, trigeminal activation, and inflammation in the trigeminal ganglion in an NTG-induced migraine model.
    METHODS AND RESULTS: Thirty male Sprague-Dawley rats were allocated to control, mitoTEMPO (M), NTG, M + NTG (concomitant administration of mitoTEMPO with NTG), and NTG + M (delayed administration of mitoTEMPO following NTG exposure) groups (n = 6/group). Serum TNF-α levels were measured by ELISA; trigeminal c-Fos, mitofusin-1 (Mfn1), nuclear respiratory factor (NRF1), and mitochondrial transcription factor A (TFAM) protein levels were assessed by Western blot, while NADH-ubiquinone oxidoreductase chain 1 (ND1), TFAM, NRF1, Mfn1, and peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) mRNA expressions were analyzed by RT-PCR. NTG administration significantly increased serum TNF-α levels and trigeminal c-Fos expression, confirming neuroinflammation and nociceptive activation. Concomitant mitoTEMPO administration attenuated c-Fos expression, whereas delayed administration had no effect, indicating a timing-dependent response. Compared with the NTG group, mitoTEMPO-treated NTG groups exhibited higher Mfn1, NRF1, and TFAM protein levels. At the transcriptional level, no differences were observed in ND1, TFAM, or NRF1 expression; however, Mfn1 mRNA was increased in the NTG group, and PGC-1α expression was significantly upregulated in the NTG + M group, consistent with a delayed mitochondrial biogenesis response.
    CONCLUSIONS: These findings suggest that NTG induces trigeminal activation and inflammation with limited acute effects on mitochondrial biogenesis, while mitoTEMPO modulates these processes in a phase-dependent manner.
    Keywords:  Migraine; MitoTEMPO; Mitochondrial biogenesis; Mitochondrial dysfunction; Trigeminal ganglion
    DOI:  https://doi.org/10.1007/s11033-026-11927-3
  29. Front Clin Diabetes Healthc. 2026 ;7 1790182
      Insulin resistance (IR) is characterized by impaired insulin signaling in skeletal muscle, liver, and adipose tissue. Increasing evidence indicates mitochondrial dysfunction as a key factor contributing to IR. Mitochondrial resilience refers to the mitochondria's ability to adapt to metabolic stress by regulating biogenesis, dynamics, mitophagy, and redox homeostasis. Linking mitochondrial resilience with insulin signaling could be essential for maintaining metabolic health. This review aims to map and synthesize the existing literature on the relationship between mitochondrial resilience and insulin resistance, focusing on cellular and molecular mechanisms, tissue-specific roles, metabolic consequences, and translational evidence from both animal and human studies. This scoping review adhered to PRISMA-ScR guidelines and included comprehensive searches of PubMed, Scopus, Web of Science, Embase, and Google Scholar. It included experimental and observational studies, original articles, systematic reviews, and meta-analyses, while excluding non-English publications and animal studies without clinical relevance. A total of 7, 012 records were identified; after removing duplicates, screening, and assessing eligibility, 184 studies were included. The evidence shows that impaired mitochondrial biogenesis, defective mitochondrial dynamics, reduced mitophagy, and oxidative stress disturb insulin signaling and promote metabolic inflexibility. Conversely, enhancing mitochondrial resilience increases mitochondrial quantity and function. Lifestyle modification strategies and pharmacological intervention target these pathways to improve mitochondrial resilience. Importantly, understanding inter-individual differences in mitochondrial adaptive capacity may support the development of personalized therapeutic and nutritional strategies aimed at improving insulin sensitivity and metabolic outcomes. In conclusion, mitochondrial resilience provides a comprehensive framework connecting mitochondrial quality to insulin signaling and metabolic health. Focusing on mitochondrial resilience is a promising, mechanism-based strategy for preventing and managing insulin resistance and its related comorbidities.
    Keywords:  insulin resistance; lifestyle interventions; metabolic health; mitochondrial biogenesis; mitochondrial dysfunction; mitochondrial resilience; mitophagy; oxidative stress
    DOI:  https://doi.org/10.3389/fcdhc.2026.1790182
  30. Burns Trauma. 2026 ;14 tkag011
       Background: Traumatic brain injury (TBI) can cause neuroinflammation and neuronal death. The role of mitochondrial dysfunction in regulating inflammasome activation during TBI remains unclear. This study aims to explore mitochondrial regulation of neuroinflammation and pyroptosis after TBI.
    Methods: We used a mouse TBI model and in vitro scratch-injured HT22 cells and primary neurons to examine changes in mitochondrial dynamics and nucleotide-binding oligomerization domain-like receptors family pyrin domain-containing 3 (NLRP3) inflammasome activation. Metformin treatment, mitofusin 1 (Mfn1) knockdown and regulation of the Mfn1 pathway were applied to evaluate the therapeutic effects and mechanisms.
    Results: TBI triggered NLRP3 inflammasome activation and neuronal pyroptosis, along with impaired mitochondrial function and oxidative stress. Metformin reduced inflammasome activation, improved mitochondrial homeostasis, and alleviated neuronal injury. These effects were lost when Mfn1 was silenced, highlighting its essential role. Furthermore, we determined that the AMPK pathway modulates these observed effects.
    Conclusion: Metformin protects against TBI-induced neuronal damage by restoring Mfn1-dependent mitochondrial dynamics and suppressing inflammasome activation. Mfn1 is a key mediator linking mitochondrial health to neuroinflammatory responses in TBI.
    Keywords:  Metformin; Mitochondrial dynamics; Mitofusin 1; NLRP3 inflammasome; Pyroptosis; Traumatic brain injury
    DOI:  https://doi.org/10.1093/burnst/tkag011
  31. Front Pediatr. 2026 ;14 1731155
       Introduction: Mycoplasma pneumoniae (M. pneumoniae) is a common community-acquired pneumonias among children and young adults. Long-term use of macrolide antibiotics treatment contributes to Macrolide-resistant M. pneumoniae (MRMP). This study aimed to investigate the roles of mitochondrial pyruvate carrier 1 (MPC1) in MRMP.
    Methods: Human coronary endothelial cells (HCAECs) were co-cultured with MRMP. mRNA expression was calculated using quantitative reverse transcriptase PCR (qRT-PCR). Protein expression was detected using Western blot. Cytokine release was detected using enzyme-linked immunosorbent assay. The morphology of mitochondria was detected using transmission electron microscopy assay. The viability of HCAECs was determined using cell counting kit-8 assay. Cytotoxicity was determined using lactate dehydrogenase cytotoxicity assay. Cell death was analyzed using terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) assay.
    Results: We found that MRMP exposure mediated mitochondrial damage and pyroptosis of HCAECs. Moreover, MPC1 was overexpressed in HCAECs exposed to MRMP. Inhibition of MPC1 promoted mitophagy as well as suppressed the pyroptosis of HCAECs. However, blocking mitophagy signaling antagonized the effects of MPC1 deficiency, resulting in mitochondrial damage and pyroptosis of HCAECs.
    Conclusion: MPC1 promotes mitochondrial damage and pyroptosis of HCAECs in MRMP through inhibiting mitophagy. Therefore, targeting MPC1 may be a promising strategy for MRMP.
    Keywords:  macrolide-resistant M. pneumoniae; mitochondrial pyruvate carrier 1; mitophagy; pyroptosis; treatment
    DOI:  https://doi.org/10.3389/fped.2026.1731155
  32. Cell Signal. 2026 May 11. pii: S0898-6568(26)00228-7. [Epub ahead of print] 112575
       BACKGROUND: The mitochondrial unfolded protein response (UPRmt) maintains proteostasis, but its dysregulation dictates cell fate. This study aimed to elucidate the signaling mechanism by which triptolide (TP), a bioactive component of Tripterygium wilfordii Hook. f., triggers hepatocellular Lipoapoptosis, focusing on HSP60-mediated UPRmt overactivation.
    METHODS: A TP-induced mouse liver injury model was established. Serum biochemistry, histopathology, and liver proteomics were performed. Key proteins (HSP60, UPRmt components, SREBP-1c, FASN, cleaved caspase-3) were validated by Western blot and RT-qPCR both in vivo and in AML-12 hepatocytes, while co-immunoprecipitation (Co-IP) was conducted in AML-12 cells. Functional validation used siRNA knockdown.
    RESULTS: TP induced liver injury, lipid deposition, and apoptosis. Proteomic screening implicated UPRmt activation, with HSP60 subsequently validated as a central upregulated component. TP downregulated MFN2 and upregulated HSP60, ClpP, DRP1, SREBP-1c, FASN, and cleaved caspase-3. Co-IP confirmed a direct HSP60-SREBP-1c interaction. Moreover, HSP60 knockdown attenuated the entire TP-induced cascade, including UPRmt overactivation, mitochondrial dysfunction, lipid dysregulation, and apoptosis.
    CONCLUSION: This study delineates a novel mitochondria-to-nucleus pathway wherein TP induces HSP60-mediated UPRmt overactivation, which promotes SREBP-1c/FASN-driven lipid accumulation, culminating in lipoapoptosis. The "HSP60-UPRmt-SREBP-1c/FASN-lipoapoptosis" axis links dysregulated organelle stress signaling to metabolic cell death. These findings establish HSP60 as a key signaling node and a potential therapeutic target for intercepting this pathological cascade.
    Keywords:  Cell signaling; HSP60; Lipoapoptosis; Mitochondrial unfolded protein response (UPR(mt)); Organelle stress; Triptolide
    DOI:  https://doi.org/10.1016/j.cellsig.2026.112575
  33. Mol Cell Endocrinol. 2026 May 13. pii: S0303-7207(26)00106-1. [Epub ahead of print] 112829
       BACKGROUND: Obesity-associated metabolic inflammation is characterized by the infiltration and pro-inflammatory polarization of adipose tissue macrophages (ATMs). Mitochondrial dysfunction represents a central pathogenic mechanism; however, the upstream molecular mechanisms that link metabolic stress to impaired mitochondrial quality control in macrophages remain inadequately defined. Regulator of G protein signaling 1 (RGS1) is significantly upregulated in ATMs under obese conditions; nevertheless, its functional role and mechanistic relevance have not been fully elucidated.
    METHODS: Integrated transcriptomic analyses identified RGS1 as a pivotal gene associated with obesity, and its expression profiles in adipose tissue macrophages were analyzed by integrating single-cell RNA sequencing data from humans and mice. In vivo, immunohistochemistry and immunofluorescence assessed RGS1 localization in adipose tissue from high-fat diet-fed obese mice. In vitro, RAW264.7 cells and bone marrow-derived macrophages (BMDMs) were treated with palmitic acid (PA) or PA plus interleukin-6 (IL-6), combined with lentivirus-mediated RGS1 knockdown. The effects of RGS1 on mitochondrial integrity, mitophagic flux, lipid metabolism, and macrophage polarization were assessed by Western blot, quantitative real-time PCR, transmission electron microscopy, TMRE staining, reactive oxygen species (ROS) production, ATP levels, and oxidative phosphorylation (OXPHOS). Furthermore, bafilomycin A1 (Baf-A1) was used to assess mitophagic flux, and Mdivi-1 was utilized to inhibit mitophagy for mechanistic validation.
    RESULTS: Bioinformatic analyses revealed a significant upregulation of RGS1 in ATMs under obese conditions. In vivo studies demonstrated elevated levels of RGS1 in the epididymal adipose tissue of obese mice, where it co-localized with CD86+ M1 macrophages. In vitro, PA treatment induced RGS1 expression and caused lipid accumulation and M1 macrophage polarization; co-stimulation with PA and interleukin-6 (IL-6) further upregulated RGS1 and exacerbated pro-inflammatory responses. Conversely, RGS1 knockdown markedly attenuated both lipid accumulation and M1 polarization. Furthermore, PA treatment induced severe mitochondrial dysfunction, characterized by cristae disruption, loss of membrane potential, ROS accumulation, ATP depletion, and decreased expression of OXPHOS complexes, and inhibited PINK1/Parkin-mediated mitophagy. In contrast, RGS1 knockdown restored mitochondrial function. Baf-A1 treatment assays confirmed that RGS1 knockdown augmented mitophagic flux, while treatment with Mdivi-1 significantly diminished this protective effect, indicating that these protective effects were likely mediated in a mitophagy-dependent manner.
    CONCLUSION: RGS1 acts as a critical switch linking metabolic stress to macrophage dysfunction. Targeting RGS1 may represent a promising therapeutic strategy for alleviating obesity-induced inflammation.
    Keywords:  Macrophage Polarization; Mitochondrial Dysfunction; Mitophagy; Obesity; PINK1/Parkin; RGS1
    DOI:  https://doi.org/10.1016/j.mce.2026.112829
  34. Arch Biochem Biophys. 2026 May 08. pii: S0003-9861(26)00114-1. [Epub ahead of print]782 110843
      Ischemia-reperfusion (I/R) injury plays a pivotal role in the pathogenesis of pressure ulcer formation. In I/R microenvironments, mitophagy serves as an essential cellular self-protection mechanism for clearing damaged mitochondria and preventing apoptosis and inflammatory responses; the HIF-1α/BNIP3 signaling pathway acts as the central hub regulating this process. Thioredoxin (TRX), a critical redox-regulatory protein, has shown protective effects in I/R-related diseases, but its role in cutaneous I/R injury remains unclear. In this study, we investigated whether recombinant human TRX (rhTRX) alleviates I/R-induced skin injury and explored the underlying mechanisms using a murine pressure ulcer model and an in vitro keratinocyte I/R model. rhTRX treatment significantly reduced tissue damage, neutrophil infiltration, and the levels of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6), the oxidative stress marker 8-OHdG, and apoptosis-related proteins (BAX, cleaved caspase-3), while increasing BCL-2 expression. Mechanistically, rhTRX suppressed intracellular ROS production and increased GSH level, it also inhibited MAPK/NF-κB signaling, thereby attenuating mitochondria-mediated inflammation and apoptosis. In addition, rhTRX preserved mitochondrial integrity by reducing cytochrome c and mitochondrial DNA release. Notably, rhTRX enhanced HIF-1α/BNIP3/LC3II-dependent mitophagy, and HIF-1α silencing partially abolished these protective effects. In conclusion, rhTRX mitigates cutaneous I/R injury by reducing oxidative stress and inflammation and by promoting mitophagy-mediated mitochondrial quality control. These findings suggest that topical TRX represents a potential therapeutic strategy for pressure ulcer prevention and treatment.
    Keywords:  Apoptosis; Inflammation; Ischemia–reperfusion injury; Mitophagy; Pressure ulcer; Thioredoxin
    DOI:  https://doi.org/10.1016/j.abb.2026.110843
  35. Exp Eye Res. 2026 May 12. pii: S0014-4835(26)00220-4. [Epub ahead of print] 111064
      Age-related macular degeneration (AMD) represents the leading cause of irreversible vision loss in the elderly, affecting over 200 million individuals worldwide. Despite recent advances, therapeutic options remain severely limited, particularly for dry AMD characterized by progressive geographic atrophy. Emerging evidence implicates mitochondrial dysfunction and metabolic reprogramming of retinal pigment epithelium (RPE) cells as central pathogenic drivers. Under pathological conditions, RPE cells exhibit profound bioenergetic collapse marked by declining oxidative phosphorylation, compensatory glycolytic activation, and aberrant tricarboxylic acid cycle intermediate accumulation. This metabolic catastrophe is structurally underpinned by dysregulated mitochondrial dynamics. The resultant accumulation of fragmented, dysfunctional mitochondria perpetuates reactive oxygen species overproduction and mitochondrial DNA damage, establishing a self-amplifying vicious cycle driving RPE degeneration. Mechanistically, this involves dysregulation of the AMPK/mTOR energy-sensing axis, SIRT1/PGC-1α transcriptional control, and Nrf2/ARE antioxidant defenses. Multi-omics profiling reveals distinct metabolic signatures. These discoveries have catalyzed mechanism-based interventions. However, translational applications still face many challenges, and the combination of single-cell multi omics and multimodal therapies is expected to play a role.in restoring mitochondrial homeostasis and preserving vision in aging population in the future.
    Keywords:  Age-related macular degeneration; Metabolic reprogramming; Mitochondrial dynamics; Mitophagy; Oxidative stress; Precision therapy; Retinal pigment epithelium
    DOI:  https://doi.org/10.1016/j.exer.2026.111064
  36. Mech Ageing Dev. 2026 May 08. pii: S0047-6374(26)00043-6. [Epub ahead of print]231 112191
      Mitochondria-lysosome contacts (MLCs) are emerging as a dynamic membrane interface that integrates organelle communication with cellular homeostasis. Rather than acting solely as intermediates of degradative trafficking, MLCs organize local calcium transfer, lipid exchange, Rab7-dependent contact remodeling, and mitochondrial quality control. These functions place MLCs at the intersection of mitochondrial fitness, lysosomal competence, metabolic adaptation, and stress signaling. Aging provides a particularly informative setting in which to examine this interface, because mitochondrial dysfunction and lysosomal decline co-emerge and reinforce one another during cellular aging. Current evidence suggests that aging does not simply increase or decrease MLCs, but instead remodels their dynamics, molecular composition, and functional output. Such remodeling may impair mitophagy, alter calcium and lipid coupling, amplify oxidative and inflammatory stress, and contribute to age-related disease phenotypes. In this review, we summarize the structural organization and regulatory logic of MLCs, examine their mechanistic roles in organelle homeostasis, and discuss how aging reshapes this interface in physiological and pathological contexts. We also highlight key methodological challenges and therapeutic opportunities for the field.
    Keywords:  Aging; Lysosome; Membrane contact sites; Mitochondria-lysosome contacts; Mitochondrial quality control; Organelle homeostasis
    DOI:  https://doi.org/10.1016/j.mad.2026.112191
  37. Front Pharmacol. 2026 ;17 1736022
      Oxymatrine (OMT) has been reported to exert neuroprotective effects in cerebral ischemia. Mitochondrial dysfunction is closely associated with the neurological deficits caused by chronic cerebral hypoperfusion (CCH). However, the potential role of mitochondrial protection in the neuroprotective effects of OMT, as well as the underlying mechanisms, remains to be fully elucidated. The present study aimed to investigate the mechanistic basis of OMT-mediated neuroprotection in vivo using a mouse model of CCH-induced cognitive impairment established by bilateral common carotid artery stenosis (BCAS), and in vitro using an HT22 cell injury model induced by oxygen-glucose deprivation/reperfusion (OGD/R). The in vivo results showed that OMT effectively alleviated CCH-induced cognitive impairment in mice. In addition, OMT treatment attenuated OGD/R-induced neuronal injury in HT22 cells. Mechanistically, OMT activated SIRT1 and promoted PINK1/Parkin-mediated mitophagy in neurons. Moreover, pharmacological inhibition of SIRT1 suppressed OMT-induced activation of PINK1/Parkin-mediated mitophagy, as well as the recovery of neuronal and cognitive function in both the cell and mouse models. These findings suggest that OMT enhances mitophagy through modulation of SIRT1, thereby ameliorating neuronal dysfunction and cognitive deficits associated with CCH and OGD/R. This study provides preclinical mechanistic evidence supporting further investigation of OMT in chronic cerebral hypoperfusion-related cognitive impairment.
    Keywords:  PINK1; chronic cerebral hypoperfusion; cognitive dysfunction; mitophagy; oxymatrine
    DOI:  https://doi.org/10.3389/fphar.2026.1736022
  38. Front Immunol. 2026 ;17 1767802
      Inflammation is a key driver of diabetic kidney disease (DKD) progression, with the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome representing a promising therapeutic target. Soluble epoxide hydrolase (sEH), an enzyme that inactivates renoprotective epoxyeicosatrienoic acids into less active diols, has been implicated in renal pathophysiology. This study investigated the role of sEH in renal tubular NLRP3 inflammasome activation and its underlying mechanisms in DKD. We observed upregulated sEH expression in high glucose (HG)-stimulated human proximal tubular epithelial (HK-2) cells and diabetic kidneys. Pharmacological inhibition of sEH attenuated diabetes-induced mitochondrial damage, mitochondrial reactive oxygen species (mtROS) production, NLRP3 inflammasome activation, and renal dysfunction both in vivo and in vitro. Furthermore, sEH inhibition restored autophagy flux and enhanced PINK1/Parkin mediated-mitophagy. Activation of mitophagy by the autophagy inducer rapamycin (Rapa) alleviated HG-induced mitochondrial impairment, mtROS overproduction, and NLRP3 inflammasome activation in HK-2 cells, suggesting that the anti-inflammatory effect of sEH inhibition is mediated through mitophagy regulation. Further mechanistic studies indicated that sEH inhibition promotes mitophagy, thereby improving mitochondrial function, reducing mtROS generation, and subsequently suppressing mtROS-dependent NLRP3 inflammasome activation in DKD. In conclusion, our findings establish a novel link between sEH and NLRP3 inflammasome activation in DKD pathogenesis, highlighting sEH inhibition as a promising therapeutic strategy for DKD treatment.
    Keywords:  NLRP3 inflammasome; diabetic kidney disease; mitochondrial reactive oxygen species; mitophagy; soluble epoxide hydrolase
    DOI:  https://doi.org/10.3389/fimmu.2026.1767802
  39. Bone Res. 2026 May 14. pii: 52. [Epub ahead of print]14(1):
      Orthodontically induced inflammatory root resorption (OIIRR) is a prevalent complication driven by excessive mechanical force, yet the underlying mechanisms linking mechanotransduction to osteoclast activation remain elusive. Here, we identify a novel signaling axis wherein sphingosine kinase 1 (SphK1) in cementocytes translates heavy orthodontic force into a pro-osteoclastogenic signal via mitophagy-mediated mitochondrial transfer. In vivo, heavy force induced OIIRR and upregulated mitophagy markers in cementocytes. In vitro, heavy compression force triggered SphK1-dependent mitophagy in IDG-CM6 cementocytes, as evidenced by increased mitophagosome formation, co-localization of mitochondria with lysosomes, and elevated PINK1/PARKIN signaling. Inhibition of SphK1, either pharmacologically or genetically, suppressed this mitophagic response. Conditioned media from force-loaded cementocytes enhanced osteoclast differentiation and glycolytic metabolism, effects that were abolished by SphK1 inhibition and rescued by a mitophagy agonist. Crucially, we demonstrated that heavy force promotes the transfer of mitochondria from cementocytes to osteoclast precursors, a process dependent on mitophagy. This transferred mitochondrial cargo functioned as a metabolic subsidy, boosting osteoclast bioenergetics and resorptive activity. Our findings unveil the SphK1-mitophagy-mitochondrial transfer axis as a fundamental mechanism of cementocyte-osteoclast communication, positioning SphK1 as a promising therapeutic target to prevent OIIRR.
    DOI:  https://doi.org/10.1038/s41413-026-00538-0
  40. Cardiol Rev. 2026 May 11.
      Mitochondria are critical cellular powerhouses that produce adenosine triphosphate to maintain the structure and integrity of the cell. Mitochondria generate 90% of the energy of a cell. Chronic inflammation causes damage to mitochondria. When enough mitochondria are dysfunctional, the involved organ will suffer. Mitochondria become dysfunctional in the setting of chronic inflammation. Under noninflammatory conditions, the body generates new mitochondria (mitochondrial biogenesis) and removes old and damaged mitochondria via mitophagy. When mitochondria are damaged, they "spontaneously" leak out reactive oxygen species, mitochondrial DNA, and damage-associated molecular patterns, generating erroneous innate immune responses. Autophagy is a recycling and housekeeping process that removes dysfunctional components, organelles, and proteins, promoting the recovery and maintenance of cell health. Mitophagy is a specific variant of this process that removes dysfunctional mitochondria from the cell. Mitophagy declines with age, allowing dysfunctional mitochondria to accumulate, and chronic inflammation leads to cardiovascular disease (CVD). In CVD, impairment of both autophagy and mitophagy leads to more chronic inflammation, characterized by hyperactivation of the nucleotide-binding oligomerization domain (NOD)-, leucine-rich repeat (LRR)- and pyrin domain-containing protein 3 (NLRP3) inflammasome, a key component of the immune system. Once activated, it triggers inflammation, leading to excessive cytokine activity, proinflammatory macrophage polarization, pyroptosis, and increased immune cell infiltration into cardiac and vascular tissues. Pyroptosis is a form of inflammatory cell death triggered by programmed cues; however, in autoimmunity and cancer, when overactivated, this process can become detrimental. Adequate regulation of these events reduces oxidative stress, inflammatory cascades, fibrosis, and maladaptive remodeling, thereby improving overall cardiovascular health. Targeted therapeutic enhancement of autophagy and mitophagy represents a promising strategy to modulate immune-driven pathology and improve outcomes in cardiovascular conditions. We will review the mechanisms of how this inflammation causes CVD.
    Keywords:  NLRP3 inflammasome; atherosclerosis; autophagy; cardiovascular disease; cytokine release; endothelial dysfunction; heart failure; immune cell infiltration; inflammasome crosstalk; inflammation; innate immunity; ischemia-reperfusion injury; macrophage polarization; mitochondrial DAMPs; mitophagy; oxidative stress; pyroptosis; redox signaling; sterile inflammation; therapeutic modulation
    DOI:  https://doi.org/10.1097/CRD.0000000000001302
  41. Ecotoxicol Environ Saf. 2026 May 11. pii: S0147-6513(26)00557-9. [Epub ahead of print]318 120228
      T-2 toxin, a type A trichothecene mycotoxin, induces severe cytotoxicity primarily through mitochondrial dysfunction and apoptosis. In this study, the protective role of astragaloside IV (AS-IV) against T-2 toxin-induced damage was investigated using the human hepatoma cell line HepG2 as an in vitro model. Our results demonstrated that T-2 toxin significantly reduced cell viability, promoted reactive oxygen species (ROS) accumulation, and impaired mitochondrial function, as evidenced by disrupted respiratory activity, loss of mitochondrial membrane potential, and reduced ATP production. These alterations were accompanied by dysregulated mitochondrial homeostasis, characterized by enhanced mitochondrial biogenesis and excessive mitochondrial fission, along with activation of the mitochondrial apoptotic pathway. Pretreatment with AS-IV mitigated ROS accumulation, rescued impaired mitochondrial respiratory function, stabilized mitochondrial membrane potential, maintained cellular ATP level, and restored mitochondrial homeostasis. Furthermore, AS-IV suppressed T-2 toxin-triggered apoptosis by modulating the BAX/BCL-2 ratio, inhibiting cytochrome c release, and attenuating caspase activation. Together, these findings indicate that AS-IV protects HepG2 cells from T-2 toxin-induced cytotoxicity by maintaining mitochondrial homeostasis and suppressing the intrinsic apoptotic pathway, providing mechanistic evidence for its protective effect.
    Keywords:  Apoptosis; Astragaloside Ⅳ; Mitochondrial dysfunction; T-2 toxin
    DOI:  https://doi.org/10.1016/j.ecoenv.2026.120228
  42. Int J Mol Sci. 2026 Apr 28. pii: 3930. [Epub ahead of print]27(9):
      Aging is a multifactorial biological process characterized by progressive functional decline and increased susceptibility to chronic diseases. Targeting the molecular mechanisms underlying aging has therefore emerged as an important strategy for promoting healthy aging. Natural polyphenols, widely present in fruits, vegetables, tea, and medical and aromatic plants, have attracted considerable attention due to their geroprotective properties. This review examines current evidence on the ability of major dietary polyphenols, including resveratrol, epigallocatechin gallate (EGCG), curcumin, and quercetin, to modulate the hallmarks of aging, with particular emphasis on mitochondrial quality control as a central regulatory mechanism. Evidence indicates that polyphenols regulate key signaling pathways involved in aging biology, including AMP-activated protein kinase (AMPK), sirtuins (SIRT), mechanistic target of rapamycin (mTOR), nuclear factor erythroid 2-related factor 2 (Nrf2), and nuclear factor-κB (NF-κB). Through coordinated modulation of these pathways, polyphenols influence mitochondrial biogenesis, mitophagy, redox homeostasis, cellular senescence, and chronic inflammation. In addition, interactions between dietary polyphenols and the gut microbiome generate bioactive metabolites, such as urolithin A, which further contribute to mitochondrial regulation. Overall, polyphenols represent promising modulators of aging-associated pathways and may support strategies aimed at improving healthspan and reducing age-related disease risk.
    Keywords:  AMPK; Nrf2; SIRT1; aging; cellular senescence; gut microbiome; inflammaging; mitochondrial quality control; mitophagy; polyphenols
    DOI:  https://doi.org/10.3390/ijms27093930
  43. Mol Cell Biochem. 2026 May 12.
      Myocardial ischemia‑reperfusion injury (I/R) is a major contributor to adverse outcomes in ischemic heart disease. Mitochondrial dysfunction plays a central role in I/R, and modulating mitophagy has shown potential in attenuating such injury. Nevertheless, whether puerarin influences mitophagy during I/R remains poorly understood. An in vivo I/R (30 min/24 h) model was established in C57BL/6 mice after 7 day puerarin pretreatment. In vitro, a hypoxia‑reoxygenation H/R (8 h/4 h) model was constructed using H9c2 cardiomyocytes. Cardiac function was assessed by echocardiography, infarct size was determined via Evans Blue‑TTC staining, mitophagy was visualized by transmission electron microscopy, and expression of mitophagy‑related proteins was evaluated by western blot. Puerarin significantly reduced I/R‑induced damage in both models. It attenuated mitochondrial depolarization and reactive oxygen species generation, increased mitophagic activity, and upregulated the mitophagy receptor FUNDC1. Puerarin alleviates myocardial ischemia‑reperfusion injury by enhancing FUNDC1‑mediated mitophagy, particularly during early reperfusion. These results reveal a key mechanism underlying the cardioprotective effect of puerarin and support its further development as a therapeutic agent for I/R.
    Keywords:  FUNDC1; Mitophagy; Myocardial ischemia-reperfusion injury; Puerarin
    DOI:  https://doi.org/10.1007/s11010-026-05567-1
  44. Neurogastroenterol Motil. 2026 May;38(5): e70341
       BACKGROUND: Slow transit constipation (STC) is a prevalent functional gastrointestinal disorder that significantly affects people's quality of life. Aurantii Fructus Immaturus (Zhishi, ZS) and Atractylodis Macrocephalae Rhizoma (Baizhu, BZ) are a classic herbal pair in traditional Chinese medicine (TCM) for regulating spleen-stomach function, respectively recognized for their properties of "replenishing qi and fortifying the spleen" and "dispersing stagnation and promoting digestion". This study aimed to elucidate the mechanisms by which ZSBZ ameliorates STC through regulating mitophagy in ICCs and restructuring gut microbiota composition.
    METHODS: A rat model of STC was established by oral gavage administration of loperamide hydrochloride (3 mg/kg·day). The therapeutic effects of ZSBZ were evaluated by assessing rat body weight, 6-h fecal number, fecal water content, and intestinal transit rate. Histopathological changes in the colon were observed using hematoxylin-eosin (HE) staining and Alcian blue-periodic acid Schiff (AB-PAS) staining. The ultrastructure of colon tissues was observed by transmission electron microscopy (TEM). Immunohistochemistry (IHC) was used to detect the expression of c-Kit, SCF, and autophagy-related markers (p62, Beclin1, and LC3II/I) in colon tissues. The expression levels of α-KGDHC and PDH were measured by ELISA. Combined with biochemical assays for SOD, MDA, respiratory chain complexes I and II, and ATP levels, a comprehensive assessment of cellular mitochondrial oxidative stress status and energy metabolism function was performed. Flow cytometry was used to quantify intracellular Ca2+ concentration and mitochondrial membrane potential (MMP) in cells isolated from colonic tissues. Mitophagy-related protein and mRNA expression were analyzed by Western blotting and reverse transcription quantitative polymerase chain reaction (RT-qPCR). Apoptosis in rat colonic tissues was detected using TUNEL assay. Gut microbiota composition was analyzed by 16S rRNA gene sequencing, and its metabolic functional potential was predicted.
    RESULTS: Our results showed that ZSBZ significantly ameliorated defecation function and enhanced intestinal motility in a rat model of STC. Histopathological and ultrastructural analyses revealed that ZSBZ effectively restored colonic mucosal damage, increased goblet cell numbers, and attenuated mitochondrial swelling with cristae disruption in ICCs of STC rats. Meanwhile, ZSBZ improved mitochondrial dysfunction by reducing MDA levels and increasing SOD activity in colonic tissues. Furthermore, ZSBZ improved mitochondrial energy metabolism by increasing ATP content, restoring respiratory chain complex I and II activities, and elevating α-KGDHC and PDH activities, thereby reversing the decline in mitochondrial membrane potential and the increase in intracellular Ca2+ concentration in cells isolated from colonic tissues. Mechanistically, ZSBZ attenuated excessive mitophagy in colonic ICCs by downregulating autophagy-related genes and proteins, restoring p62 expression, and suppressing the elevated mRNA and protein expression of the mitophagy-related markers PINK1 and Parkin. In addition, 16S rRNA gene sequencing demonstrated that ZSBZ reshaped the gut microbiota in STC rats, characterized by a decreased abundance of Proteobacteria and an increased abundance of Bacteroidota. KEGG functional prediction further indicated that ZSBZ regulated mitochondrial metabolism-related pathways, possibly contributing to the amelioration of colonic dysmotility.
    CONCLUSION: ZSBZ significantly alleviated constipation symptoms in STC rats. The mechanism may involve inhibition of excessive mitophagy in ICCs and restructuring of gut microbiota composition. This study provides compelling theoretical support for ZSBZ as a therapeutic strategy against STC and offers novel insights into intestinal motility restoration in humans.
    Keywords:   Atractylodis Macrocephalae Rhizoma ; Aurantii Fructus Immaturus ; gut microbiota; mitophagy; slow transit constipation
    DOI:  https://doi.org/10.1111/nmo.70341
  45. Nat Aging. 2026 May 14.
      ULK1 (Atg1) initiates macroautophagy and mitophagy, which support neuronal growth and survival, yet how this pathway is disrupted in aging and Alzheimer's disease (AD) remains unclear. Here we report reduced ULK1 in serum and cerebrospinal fluid during aging in cognitively unimpaired participants from the COGNORM study (n = 75) and in patients with AD from the NorCog Memory Clinic Cohort (n = 316). In AD mice, ULK1 overexpression stimulates autophagic flux, reduces AD pathology and delays cognitive decline alongside increased phagocytic degradation of amyloid-β, reduced tauopathy and improved mitochondrial quality. Mechanistically, ULK1 upregulation increases autophagy and PINK1-, FUNDC1- and AMBRA1-associated mitophagy; higher autophagy and mitophagy increase cellular NAD+, which in turn deacetylates acetylated-Tau174 via the NAD+-SIRT1 axis, leading to reduced tauopathy. Using in vitro tau seeding assays and a Caenorhabditis elegans tau model, we validate the efficacy of ULK1 activators in inhibiting tauopathy. We propose that age-related decline in ULK1 leads to autophagy and mitophagy impairment and increases the progression of AD and identify ULK1 as a potential therapeutic target.
    DOI:  https://doi.org/10.1038/s43587-026-01108-z
  46. PLoS One. 2026 ;21(5): e0348274
      Acute gouty arthritis (AGA) is a common inflammatory joint disease characterized by pain resulting from the deposition of monosodium urate (MSU) crystals into joints and surrounding tissues. RGFP966, a selective inhibitor of histone deacetylases 3 (HDAC3), can down-regulate the AIM2 inflammasomes. This study aimed to explore the mechanism of action of RGFP966 in MSU-induced AGA. MSU-induced AGA rats were treated with RGFP966 or colchicine, and physiological and pathological indicators were determined. The rat joint synovial tissues and kidneys pathological damage was observed by hematoxylin and eosin staining. Enzyme-linked immunosorbent assay (ELISA), Western blot, JC-1 staining, mitochondrial membrane potential (MMP) measurement, ATP assay, and immunofluorescence were applied to evaluate the effects of RGFP966 on the AIM2 inflammasomes and mitophagy. In MSU-induced AGA rats, RGFP966 significantly improved the gait score, the swelling degree and synovitis score. In addition, RGFP966 repressed the increased serum levels of IL-1β, IL-18, IL-6 and TNF-α, and reduced the protein levels of AIM2, Pro-caspase-1, Cleaved-caspase-1, ASC, Pro-IL-1β, and Cleaved-IL-1β in MSU-induced AGA rats. Furthermore, RGFP966 decreased the level of reactive oxygen species (ROS), increased the level of ATP and MMP, and promoted the levels of Pink1, Parkin and LC3-II. Collectively, RGFP966 significantly alleviated AGA, and the underlying mechanism is related to promote mitophagy by inhibiting the activation of the AIM2 inflammasomes.
    DOI:  https://doi.org/10.1371/journal.pone.0348274
  47. EMBO Rep. 2026 May 14.
      Mitochondrial biogenesis and inheritance must be tightly coordinated with cell division to maintain mitochondrial function and cell survival. The dynamics of the mitochondrial network, including fusion and fission, are essential for mitochondrial inheritance and quality control. In budding yeast, simultaneous inhibition of both processes compromises mitochondrial DNA (mtDNA) integrity, increasing the frequency of petite cells. Loss of fusion alone completely eliminates mtDNA. Although this has been known for decades, why mtDNA is lost remained unclear. Here, we examine the effects of impaired mitochondrial fusion by depleting the mitofusin Fzo1. By analyzing over thirty thousand single cells across their cell cycles, we show that Fzo1-depletion induces rapid mitochondrial fragmentation and loss of membrane potential, followed by progressive declines in mtDNA content and growth rate. During division, Fzo1-depleted daughters inherit disproportionately large mitochondrial amounts, leaving mothers with too little. This imbalance, combined with an inability to upregulate compensatory mtDNA synthesis, drives rapid mtDNA loss. Our results reveal how fusion defects cause mtDNA loss and mitochondrial dysfunction, which might have implications for diseases linked to impaired fusion.
    DOI:  https://doi.org/10.1038/s44319-026-00794-5
  48. Clin Epigenetics. 2026 May 12.
       BACKGROUND: METTL3 is a pivotal N6-methyladenosine (m⁶A) regulator that is linked to a worse prognosis of colorectal cancer (CRC). However, METTL3's oncogenic molecular networks in CRC remain unclear. This study aims to establish a co-expression network of METTL3 and identify novel diagnostic and therapeutic targets for CRC.
    METHODS: We integrated transcriptomic datasets with clinical cohorts and patient-derived organoids (PDOs) to evaluate the expression profiles of METTL3 and PRMT5. Mechanistic insights were gained through co-immunoprecipitation (Co-IP), m⁶A-methylated RNA immunoprecipitation (MeRIP), and Quantitative real-time PCR (qRT-PCR) assays. Single-cell and spatial transcriptomics were employed to resolve their spatial co-localization and cellular architecture. Furthermore, we performed patient stratification based on the METTL3/PRMT5 axis to characterize tumor microenvironment (TME) remodeling. The functional roles of these proteins in cell proliferation, mitochondrial fission, and mitophagy were validated in CRC cells and PDOs. Finally, the synergistic efficacy of the METTL3 inhibitor STM2457 and the PRMT5 inhibitor GSK591 was evaluated.
    RESULTS: We identified a reciprocal positive feedback loop between METTL3 and PRMT5 that drives CRC malignancy: PRMT5 enhances METTL3 stability via symmetric dimethylarginine modification, while METTL3 facilitates PRMT5 expression in an m⁶A-dependent manner. Spatial and single-cell analysis revealed that their co-expression is spatially restricted and strongly correlates with an immunosuppressive TME. High METTL3/PRMT5 expression defines a specific molecular subtype characterized by accelerated cell cycle progression, DNA replication, and aberrant organelle fission. Critically, these phenotypes were functionally validated, showing that the METTL3/PRMT5 axis governs mitochondrial homeostasis. From a clinical perspective, CRC cell lines and PDOs with high METTL3/PRMT5 expression exhibited heightened sensitivity to combined inhibition with STM2457 and GSK591, revealing a potent therapeutic vulnerability.
    CONCLUSION: Our findings establish METTL3 and PRMT5 as a pair of robust biomarkers for patient stratification and highlight the synergistic targeting of m⁶A and protein methylation as a promising precision oncology strategy for CRC.
    Keywords:   METTL3 ; PRMT5 ; Colorectal cancer; Mitophagy; m⁶A
    DOI:  https://doi.org/10.1186/s13148-026-02144-7
  49. Trends Cell Biol. 2026 May 13. pii: S0962-8924(26)00065-6. [Epub ahead of print]
      Mitochondria divide and fuse, and the balance between these processes maintains mitochondrial morphology and function. Although the core fusion and division machinery is well established, how cells sense mitochondrial morphology and actively adjust it remains unclear. In this Opinion article, we propose a new conceptual framework, termed 'Mitochondrial Safeguard (MitoSafe)', in which cells monitor mitochondrial size and rebalance division and fusion through four branches: activation of fusion or inhibition of division in small mitochondria and activation of division or inhibition of fusion in enlarged mitochondria. Recent findings show that fusion is suppressed once mitochondria exceed a healthy size threshold. Dysregulation of this branch of MitoSafe, involving Parkin, PINK1, SLC25A3, SOD1, and cytochrome-c oxidase, causes mitochondrial enlargement, mitochondrial DNA release, and stimulator of interferon genes (STING)-mediated inflammation.
    Keywords:  OMA1; PINK1; Parkin; dynamin-related GTPase; inflammation; mitochondria
    DOI:  https://doi.org/10.1016/j.tcb.2026.04.007
  50. Health Sci Rep. 2026 May;9 e72501
       Background: The apoptotic pathway mediated by mitochondria depends on the activation of pro-apoptotic Bcl-2 proteins Bax and Bak. When they permeabilize the outer mitochondrial membrane (OMM), mitochondrial dysfunction occurs, leading to caspase activation. A recent study proposed that Bax accumulation on mitochondria increases apoptotic susceptibility, with adhesion-initiated signals regulating Bax. When adhesion signaling is inhibited, Bax translocates to the OMM, undergoes conformational change, and forms complexes that create pores. Although MOMP is well studied, mechanisms regulating Bax shuttling, non-canonical partners, and mitochondrial dynamics remain poorly understood.
    Aims: This review aims to provide insights by discussing the mechanisms through which Bax regulates its mitochondrial targeting, the mitochondrial dynamics associated with Bax translocation, and their influence to apoptosis. Understanding these processes could reveal new insights into the decision-making checkpoints that determine cell death.
    Methods: A comprehensive literature search was conducted across scientific databases for peer-reviewed publications up to 2025. Search terms included Bax retrotranslocation, mitochondrial dynamics, Bcl-2 family interactome, and apoptotic priming.
    Results: Recent evidence shows that Bax continuously retrotranslocates from mitochondria to the cytosol under survival conditions, a process driven by anti-apoptotic Bcl-2 proteins. When adhesion signaling or other survival cues are inhibited, this cycle is disrupted, leading to Bax accumulation on mitochondria, its oligomerization, and the onset of MOMP. Several mitochondrial proteins, including Drp1, MAVS, OCIAD1, PTPN1, and AKAP1, have also been linked to a mitochondrial interaction network that influences Bax localization and retrotranslocation. Proximity-labeling approaches such as BioID are further identifying new proteins that may regulate Bax's mitochondrial targeting and apoptotic priming.
    Conclusion: The mechanisms driving Bax accumulation on mitochondria and its retrotranslocation remain unclear, especially the role of mitochondrial proteins. Evidence suggests mitochondrial interaction networks influence Bax and Bak regulation. Further research is needed to define how these networks integrate with the Bcl-2 interactome to shape apoptotic decisions.
    Keywords:  Bax retrotranslocation; Bcl‐2 family proteins; apoptotic priming; cell death regulation; mitochondrial dynamics; mitochondrial outer membrane permeabilization (MOMP); protein–protein interaction networks; pro‐apoptotic signaling
    DOI:  https://doi.org/10.1002/hsr2.72501
  51. Biochem Biophys Rep. 2026 Jun;46 102602
      Allergic rhinitis (AR) is a type 2 inflammation-related disease, potentially associated with innate lymphoid cells (ILC2s), nasal microbiota, and autophagy. Mice were divided into control, AR, AR + IL-33, and AR + antibiotic groups(n = 5). ELISA was used to measure IL-4, IL-5, and IL-13, Masson staining to evaluate tissue remodeling, flow cytometry to detect ILC2s and memory ILC2s, 16S rRNA sequencing to analyze nasal microbiota, and Western blot to assess autophagy and mitophagy proteins. Compared with controls, mice in each AR group exhibited more nasal symptoms, enhanced tissue remodeling, and altered microbiota diversity with reduced Proteobacteria and increased Firmicutes. IL-33 further elevated type 2 cytokines in serum and nasal lavage fluid, increased nasal ILC2s and miR-155 expression, but did not affect memory ILC2s. All treatment groups showed increased p62 and LC3II/LC3I ratio, along with decreased FUNDC1 and BNIP3L levels. These findings suggest that AR is characterized by type 2 inflammation, tissue remodeling, and microbial dysbiosis, with IL-33 aggravation. Autophagy and mitophagy dysfunction may contribute to AR pathogenesis.
    Keywords:  16S rRNA; Allergic rhinitis; Autophagy; ILC2s; Mitophagy; Type 2 cytokines
    DOI:  https://doi.org/10.1016/j.bbrep.2026.102602
  52. Curr Neuropharmacol. 2026 May 08.
      Alzheimer's disease (AD) is the primary cause of dementia, characterized by a progres-sive decrease in mental abilities and the accumulation of amyloid-beta (Aβ) peptides in the brain. The combination of these peptides leads to the development of neuritic plaques and neurofibrillary tangles that disrupt neural communication and eventually lead to the loss of neurons. One of the fac-tors that are involved in the development of AD is mitochondrial dysfunction. Disrupted function-ing of mitochondria leads to the production of less energy by the cells, increased oxidative stress, and accelerates the neurodegeneration process. Neurons that carry out their mitochondrial functions normally are required to keep the balance of calcium, in a reasonable energy production, and in the survival of the cells. Mitophagy, which guarantees the clearing of damaged mitochondria, is im-paired in AD. Cholinesterase blockers and NMDA receptor blockers are currently used as treat-ments, but these are not aimed at the underlying pathophysiology of the condition. New treatment approaches that are aimed at enhancing mitochondrial health, in contrast, are viable at providing a potential to decelerate or alter mitochondrial AD progression. The goals of these approaches include enhancement of the mitophagy process, alleviation of oxidative stress, and preservation of mito-chondrial health, which may disrupt major pathological events such as Aβ aggregation and tau hy-perphosphorylation. By concentrating on the replacement of mitochondria, scientists are moving in the right direction to develop therapies that will not only help control the symptoms but also cure the disease.
    Keywords:  Alzheimer’s disease; antioxidants; calcium dyshomeostasis; mitochondrial dysfunction; mitochondrial targeted therapies; mitophagy; neurodegeneration; neuroprotection; oxidative stress.
    DOI:  https://doi.org/10.2174/011570159X419571260226033536
  53. Cell Death Dis. 2026 May 13.
      Regulator of calcineurin 1 (RCAN1) is an RNA-binding protein with diverse functions, the regulatory mechanisms underlying mitochondrial function in ischemic neuronal injury remain only partially understood. This study identified significantly elevated plasma RCAN1.1 levels in acute ischemic stroke (AIS) patients and demonstrated that mitochondrial translocation of RCAN1.1L ‌within the ischemic penumbra‌ aggravates cerebral infarction ‌by promoting pathological mitochondrial fission and neuronal apoptosis‌. Mechanistically, in AIS cell and mouse models, multi-omics screening identified activating transcription factor 2 (ATF2) mRNA as a critical downstream target of RCAN1.1L. RCAN1.1L binds to the 2915-2935 nucleotide in the 3'-untranslated region (UTR) of ATF2 mRNA, stabilizing its expression and promoting the accumulation of mitochondrial ATF2 (mtATF2) protein. MtATF2, in turn, binds to and upregulates mitochondrial fission 1 (FIS1) protein, thereby enhancing mitochondrial fission and driving intrinsic apoptosis. Notably, the RNA aptamer R1SR13 competitively binds to RCAN1.1L protein with ATF2 mRNA, exerting neuroprotective effects by disrupting the RCAN1.1L-mtATF2-FIS1 axis. These findings identify RCAN1.1L as an upstream regulator of ATF2 mRNA stability-mediated mitochondrial fission and apoptosis in ischemic penumbra neurons and highlight R1SR13 as a promising therapeutic candidate for preserving neuronal mitochondrial integrity.
    DOI:  https://doi.org/10.1038/s41419-026-08809-8
  54. Endokrynol Pol. 2026 May 15.
       INTRODUCTION: Hyperglycemia-induced endothelial injury is a major contributor to diabetic vasculopathy. While sodium-glucose transporter2 (SGLT2) in renal proximal tubules plays a critical role in diabetes, its expression and function in kidney endothelial cells, particularly regarding sex-specific disease progression, remain unclear.
    MATERIAL AND METHODS: SGLT2 expression in kidney endothelial cells was examined in male streptozotocin (STZ)-induced diabetic miceusing immunostaining. In human umbilical vein endothelial cells (HUVECs) treated with high glucose, we investigated the impact ofSGLT2 on mitochondrial dynamics following empagliflozin treatment. Molecular mechanisms were elucidated using qRT-PCR and Westernblot. Therapeutic efficacy was evaluated by histological analysis.
    RESULTS: SGLT2 was significantly upregulated in kidney endothelial cells of diabetic male mice. High glucose increased SGLT2 expressionin HUVECs, promoting mitochondrial fission and reducing fusion. Both SGLT2 siRNA knockdown and empagliflozin treatment markedlyenhanced mitochondrial fusion. Mechanistically, empagliflozin activated AMPK, increasing KLF4 expression and promoting mitochondrialfusion, thereby protecting against endothelial dysfunction. AMPK inhibition abrogated empagliflozin's protective effects in diabetic mice.
    CONCLUSIONS: SGLT2 critically regulates endothelial dysfunction under hyperglycemic conditions through the AMPK/KLF4-mitochondrialdynamics axis. Empagliflozin protects both proximal tubules and kidney endothelial cells in diabetes. Given accelerated diabetic kidneydisease progression in males, our male mouse model findings provide clinically relevant insights into sex-specific therapeutic responsesto SGLT2 inhibitors in diabetic vasculopathy.
    Keywords:  AMPK; KLF4; SGLT2; empagliflozin; mitochondria dynamics
    DOI:  https://doi.org/10.5603/ep.110841
  55. Adv Sci (Weinh). 2026 May 12. e75666
      Diabetic osteoporosis (DOP) is a chronic complication of diabetes mellitus characterized by reduced bone mass, disrupted microarchitecture, and an elevated fracture risk. Persistent oxidative stress and inflammation further inhibit osteogenesis and angiogenesis, accelerating bone degeneration. In this study, we used a peptide-polyphenol conjugation strategy to develop a multifunctional colloidal nanoplatform (β-GP@EGCG-E7). The bone-targeting peptide E7 was covalently conjugated with epigallocatechin-3- gallate (EGCG) and subsequently loaded with β-glycerophosphate (β-GP). Sequentially, this nanoplatform integrates bone-targeted delivery, improving mitochondrial quality by anti-inflammation and antioxidation, as well as osteogenesis and angiogenesis within a single system. In detail, in a high glucose microenvironment, the nanoplatform selectively accumulates in bone lesions, scavenges excess intracellular reactive oxygen species (ROS) triggered by high glucose, clears damaged mitochondria by activating PINK1-Parkin mediated mitophagy, and exerts anti-inflammatory effects to rebalance the microenvironment of bone regeneration. Concurrently, sustained phosphate release supports mineralization, promotes osteogenic differentiation, enhances angiogenesis, and improves local microcirculation. In diabetic osteoporotic models, β-GP@EGCG-E7 significantly reduced oxidative stress, restored mitochondrial homeostasis, and promoted bone and vascular regeneration. This study provides a promising therapeutic strategy for DOP and highlights the potential of peptide-polyphenol hybrid nanomaterials for regenerative applications.
    DOI:  https://doi.org/10.1002/advs.75666
  56. Ageing Res Rev. 2026 May 07. pii: S1568-1637(26)00149-2. [Epub ahead of print]119 103157
      Alzheimer's disease (AD) is the most common neurodegenerative disorder worldwide and the leading cause of dementia in older adults. The presence of extracellular β-amyloid (Aβ) plaques and intracellular neurofibrillary tangles (NFTs) constitutes the two principal neuropathological features of AD. However, current therapies targeting only Aβ or tau remain suboptimal, likely due to intrinsic neuronal and glial dysfunction in affected brain regions. Urolithin A (UroA) is a widely recognized mitophagy activator with potent antioxidant and anti-inflammatory properties. Current clinical studies confirm UroA's safety in humans and its broad benefits for mitochondrial health. Preclinical data show enhanced lysosomal and mitochondrial quality in neurons and glia during AD progression. Given current AD pathology insights, UroA shows significant therapeutic promise. The AMPK/SIRT/mTOR signaling axis regulates cellular adaptation to metabolic stress and energy balance, and is significantly dysregulated in AD progression. This review comprehensively evaluates the structural and biological characteristics of UroA, with a focus on its role in enhancing mitophagy, promoting lysophagy, and mitigating neuroinflammation in the context of AD. However, current research has not clarified how UroA enhances mitochondrial and lysosomal function while suppressing neuroinflammation. This report further investigates the potential interplay between UroA and the AMPK/SIRT/mTOR signaling pathway, elucidating a plausible mechanism through which UroA regulates the autophagic-lysosomal system and mitigates neuroinflammation via modulation of this axis.
    Keywords:  Alzheimer's disease; Lysophagy; Mitophagy; Neuroinflammation; Urolithin A
    DOI:  https://doi.org/10.1016/j.arr.2026.103157
  57. Nat Prod Res. 2026 May 14. 1-9
      This study investigates the therapeutic potential and underlying mechanisms of triterpenoids (TR) derived from the leaves of Astragalus mongholicus Bunge for the treatment of Alzheimer's disease (AD). Eighteen triterpenoid compounds were identified in the TR fraction using UPLC-Q-TOF-MS. In the 3 × Tg-AD transgenic mouse model, the therapeutic efficacy of TR was assessed using a comprehensive approach that included the Morris water maze, histopathological analysis, transmission electron microscopy, and Western blotting. The findings revealed that TR significantly improved spatial learning and memory impairments, reduced hippocampal neuronal degeneration, and diminished the deposition of phosphorylated Tau (p-Tau) protein. Ultrastructural examination further confirmed that TR preserved mitochondrial integrity. Mechanistic studies showed that TR upregulated key mitophagy-related proteins in both PINK1/Parkin-dependent and -independent pathways. In conclusion, TR exerts neuroprotective effects by activating mitophagy through multiple pathways, highlighting its potential as a promising therapeutic candidate for AD. This study not only provides experimental evidence for the therapeutic potential of natural products targeting mitophagy in Alzheimer's disease but also expands the medicinal development value of the leaves of Astragalus mongholicus Bunge.
    Keywords:  Alzheimer’s disease; mitochondrial autophagy; triterpenoids from the leaves of Astragalus mongholicus Bunge
    DOI:  https://doi.org/10.1080/14786419.2026.2671969
  58. ACS Appl Mater Interfaces. 2026 May 13.
      Severe oxidative stress, persistent inflammation, and mitochondrial dysfunction during the secondary injury phase of spinal cord injury (SCI) severely impede regeneration. Here, we report a supramolecular hydrogel, Que@MCEu/H, engineered by metal-phenolic coordination between Quercetin (Que) and mesoporous Ce-doped europium oxide nanozymes (MCEu). This injectable system integrates the CAT/SOD-mimicking activities of MCEu with the therapeutic benefits of Que to achieve a multitargeted SCI intervention. In vitro, Que@MCEu/H efficiently scavenges reactive oxygen species, preserves mitochondrial ultrastructure, inhibits apoptosis, and drives macrophage polarization from M1 to M2, thereby remodeling the inflammatory microenvironment and alleviating oxidative-stress-induced neurite retraction. In vivo, Que@MCEu/H markedly reduces lesion cavities and fibrotic scarring in a mouse contusion SCI model, suppresses GFAP-positive glial scar formation, and promotes axonal regeneration and angiogenesis, culminating in improved locomotor function. Mechanistically, therapeutic outcomes correlate with upregulation of autophagy/mitophagy markers (Beclin-1, Parkin, LC3B), indicating enhanced clearance of damaged mitochondria and neuronal protection. Collectively, Que@MCEu/H offers a promising, multifunctional platform that couples antioxidation, immunomodulation, and mitochondrial protection to facilitate SCI repair and functional recovery.
    Keywords:  hydrogel; mitophagy; nanozyme; neuroregeneration; spinal cord injury
    DOI:  https://doi.org/10.1021/acsami.6c03907
  59. Genet Res (Camb). 2026 ;2026(1): e5579542
      Mitophagy is essential for cancer formation and invasion, but its role in colorectal cancer (CRC) remains unclear. We obtained sequencing data and mitophagy-related genes (MP-RGs) from public databases. Differential expression analysis and weighted gene coexpression network analysis (WGCNA) identified mitophagy-related differentially expressed genes (DE-MPGs). Mendelian randomization (MR) analysis identified candidate genes with genetically supported causal relevance to CRC. Biomarkers were identified using machine learning, receiver operating characteristic (ROC) analysis and expression studies. Single-cell RNA sequencing (scRNA-seq) analyzed biomarker expression profiles in various CRC cell types. Quantitative PCR (qPCR) validated biomarker expression in clinical CRC samples. 147 DE-MPGs were identified. MR analysis revealed seven genes with potential causal contributions to CRC susceptibility. Three genes, SGCE (IVW: OR = 1.00041, p = 0.011), ATP8B2 (IVW: OR = 0.99920, p = 0.042), and RANGAP1 (IVW: OR = 0.99861, p = 0.002), were selected as biomarkers. Immune microenvironment and checkpoint differences were observed between CRC and controls. Biomarker expression varied among cell types. qPCR showed decreased SGCE and ATP8B2 and increased RANGAP1 in CRC. SGCE, ATP8B2, and RANGAP1 can serve as mitophagy-related biomarkers with genetically supported causal relevance to CRC, providing new insights for CRC diagnosis and therapy.
    Keywords:  biomarkers; colorectal cancer; mitophagy; single-cell RNA sequencing; two-sample Mendelian randomization
    DOI:  https://doi.org/10.1155/genr/5579542
  60. Aging Cell. 2026 05;25(5): e70508
      FAM162A is an inner mitochondrial protein known for its role in hypoxia-induced apoptosis. However, it is often overexpressed in cancer, where its pro-apoptotic function appears to be overridden, suggesting novel unknown roles in mitochondrial function and cell survival. Furthermore, its precise localization, topology, and orientation remain controversial. In this study, we aimed to assess the role of FAM162A in mitochondrial structure, dynamics, and bioenergetics and its impact on cellular and organismal stress resistance, while also establishing its localization, topology, and orientation. To this end, localization, topology, and orientation were determined by protease-protection assays in COS7 cells. In vitro loss- and gain-of-function experiments assessed mitochondrial structure and function by confocal microscopy, immunoblotting, and Seahorse analysis, while a transgenic Drosophila model overexpressing human FAM162A was generated to evaluate organismal survival under normal and heat stress conditions. We found that FAM162A localized to the inner mitochondrial membrane, predominantly within the cristae, and supported cristae ultrastructure, bioenergetics, and mitochondrial turnover, thereby enhancing oxidative metabolism, cell viability, and stress resistance. FAM162A expression was positively associated with the fusion protein OPA1 and interacted with OPA1 to regulate the proportion of long- and short-OPA1 isoforms. Transgenic Drosophila overexpressing human FAM162A exhibited increased lifespan and locomotor activity under both normal and heat stress conditions. Overall, FAM162A emerges as a key regulator of mitochondrial integrity and bioenergetics through its association with OPA1, confirming a novel role in cellular health and stress resistance.
    Keywords:  FAM162A; HGTD‐P; OPA1; bioenergetics; mitochondrial dynamics; stress resistance
    DOI:  https://doi.org/10.1111/acel.70508
  61. Nat Commun. 2026 May 13.
      Mitochondrial function critically depends on protein quality control systems, with the m-AAA protease playing a key role at the inner mitochondrial membrane (IMM). The evolutionarily conserved prohibitins (PHBs) are essential modulators of this protease across species, yet the molecular mechanisms remain unclear. Here, we present the cryo-EM structure of the Chaetomium thermophilum PHB (CtPHB) complex, revealing a cage-like assembly composed of 11 copies of PHB1/PHB2 heterodimers. Electron microscopic and biochemical analyses suggest that m-AAA proteases are enclosed within the PHB complex through interactions mediated by their SPFH-interacting motif (SIM) exposed in the intermembrane space. Further in situ cryo-ET directly visualizes these cage-protease assemblies in native mitochondria. Disruption of their interface leads to elevated m-AAA protease activity and diminished mitochondrial stress resistance. These data establish PHB complexes as spatial organizers that compartmentalize m-AAA proteases in membrane microdomains to fine-tune proteolytic homeostasis. Our findings reveal the critical role of the PHB complex in maintaining mitochondrial proteostasis, providing a unified mechanistic model to explain and reconcile the pleiotropic and often contradictory phenotypes of PHB and m-AAA protease in mitochondrial physiology and various disease conditions.
    DOI:  https://doi.org/10.1038/s41467-026-73040-0
  62. Cancer Res Treat. 2026 May 12.
       Purpose: Genome-wide association studies (GWASs) have identified single-nucleotide polymorphisms (SNPs) at the 6p21.1 locus associated with gastric cancer (GC) risk. However, the underlying biological mechanisms remain poorly understood.
    Materials and Methods: We conducted fine-mapping analysis of the 6p21.1 region using large-scale GC GWAS data (10,254 cases and 10,914 controls). Functional annotation, luciferase reporter assays, Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) experiments were performed to identify functional variants. The eQTL and colocalization analyses were used to determine the susceptibility gene. Mechanistic investigations included phenotypic assays under normoxic and hypoxic conditions, along with seahorse, immunofluorescence and ATP assays to assess mitochondrial function.
    Results: We identified rs9381024 as the independent association signal at 6p21.1, with rs2235679, in strong linkage disequilibrium with rs9381024, emerging as a potential causative SNP. The T risk allele of rs2235679 reduced APOBEC2 expression by enhancing the binding of transcriptional repressor MZF1, thereby suppressing promoter activity. Expression analysis revealed a progressive decrease in APOBEC2 levels with gastric lesions severity, becoming nearly undetectable in GC tissues. Functionally, reduced APOBEC2 expression significantly promoted the proliferation of GC cells under hypoxic conditions but not under normoxia. Mechanistically, downregulation of APOBEC2 activated mitophagy to maintain mitochondria homeostasis via HIF-1α/BNIP3 pathway under hypoxia, ultimately driving tumor growth.
    Conclusion: Our findings provide novel mechanistic insights into how genetic variants at 6p21.1 contribute to GC risk and progression, highlighting the tumor-suppressive role of APOBEC2.
    Keywords:  6p21.1; APOBEC2; Mitophagy; Stomach neoplasms; Susceptibility
    DOI:  https://doi.org/10.4143/crt.2025.1194
  63. Free Radic Biol Med. 2026 May 07. pii: S0891-5849(26)00459-4. [Epub ahead of print]
       OBJECTIVE: The induced membrane technique is a clinical strategy for managing large bone defects, which relies on endochondral ossification. However, the metabolic mechanisms regulating this process remain largely uncharacterized. We utilized scRNA-seq to analyze chondro-osseous dynamics during membrane-induced osteogenesis, with a specific focus on the role of FMO1.
    METHODS: Following the scRNA-seq profiling of human induced membranes, FMO1 function was examined using in vivo and in vitro models of triiodothyronine (T3)-induced chondrocyte hypertrophy. Mechanistic investigations incorporated FMO1 genetic knockdown and overexpression, pharmacological inhibition (methimazole), targeted mitochondrial functional assays, and senolytic clearance (ABT-263).
    RESULTS: FMO1, an enzyme typically associated with xenobiotic metabolism, was upregulated during chondrocyte hypertrophy. Both T3 stimulation and direct FMO1 overexpression increased intracellular and mitochondrial reactive oxygen species. This localized oxidative stress altered mitochondrial homeostasis by shifting organelle dynamics toward fission, characterized by Drp1 upregulation and Mfn1/2 downregulation. This structural imbalance induced cellular senescence via the p16/p21 axis, resulting in abnormal matrix mineralization and increased expression of catabolic markers (COL10A1, MMP13). Genetic knockdown or pharmacological inhibition of FMO1, as well as the clearance of senescent cells, reduced these hypertrophic and senescent phenotypes.
    CONCLUSIONS: We describe an FMO1-ROS-mitochondria axis that links metabolic oxidative stress to chondrocyte senescence. While baseline FMO1 expression occurs during physiological bone repair, its sustained activation drives pathological calcification and cartilage degeneration. Targeting this axis presents a potential biological strategy for modulating the osteogenic microenvironment and managing cartilage disorders.
    Keywords:  Chondrocyte degeneration; flavin-containing monooxygenase1; mitochondrial functional stability,reactive oxygen species(ROS); single-cell RNA sequencing
    DOI:  https://doi.org/10.1016/j.freeradbiomed.2026.04.158
  64. Biomaterials. 2026 May 07. pii: S0142-9612(26)00305-4. [Epub ahead of print]334 124281
      The refractory nature of periodontitis stems from two interrelated factors: the difficulty in eradicating deeply entrenched pathogenic biofilms and the biofilm-induced impairment of mitochondrial autophagy in immune cells, leading to metabolic dysregulation and persistent inflammation. These processes mutually reinforce each other, creating a self-perpetuating vicious cycle. To address this, we developed a spatiotemporally programmable smart hydrogel (GM hydrogel), constructed on a dynamically crosslinked network of oxidized fucoidan and carboxymethyl chitosan, loaded with silver nanoparticles and EGCG-modified MXene nanosheets (MXene@EGCG-Ag). This near-infrared (NIR) light-responsive platform exhibits excellent injectability, enabling it to completely fill narrow, deep, and irregular periodontal pockets, ensuring intimate contact with pathological sites. The GM hydrogel provides programmed control along both temporal and spatial dimensions. In the temporal dimension, NIR irradiation triggers MXene-mediated mild photothermal effects (<45 °C) that disrupt biofilm structure and facilitate Ag+ and EGCG penetration into deeper tissues. In subsequent stages, sustained EGCG release restores mitochondrial autophagy, reprogramming immune cell metabolism to improve the immune microenvironment. Spatially, the hydrogel penetrates mature biofilms and delivers comprehensive treatment from the surface through deep gingiva to the alveolar bone interface. Experimental results demonstrate that GM hydrogel disrupts ionic homeostasis and impairs biofilm functionality in Porphyromonas gingivalis, exhibiting potent antibacterial effects. Sustained EGCG release activates the PINK1/Parkin-mediated FOXO pathway, which restores mitochondrial autophagy and induces metabolic reprogramming, thereby suppressing inflammation and promoting alveolar bone regeneration.
    Keywords:  Injectable hydrogel; Mitochondrial autophagy; Oral microbiota regulation; Periodontitis
    DOI:  https://doi.org/10.1016/j.biomaterials.2026.124281
  65. Int Immunopharmacol. 2026 May 13. pii: S1567-5769(26)00685-5. [Epub ahead of print]182 116839
      Ferroptosis of cardiomyocytes is a key factor in myocardial ischemia-reperfusion injury (MIRI), but its regulatory mechanisms and intervention targets have not been fully clarified. Calcitonin gene-related peptide (CGRP) is a key regulatory factor released from peripheral vascular nerve endings, with powerful vasodilatory, positive chronotropic, and inotropic effects. In this study, the effects of CGRP on myocardial ischemia/reperfusion injury (I/R) and hypoxia/reoxygenation (H/R) were investigated in a rat model of left anterior descending coronary artery ligation and reperfusion. We found that the endogenous CGRP concentration in the serum of I/R rats was significantly decreased. While exogenous CGRP improved the viability of H/R cardiomyocytes in a concentration-dependent manner, inhibited the release of lactate dehydrogenase, down-regulated the expression of ferroptosis executive protein ACSL4, up-regulated the expression of GPX4, and reduced the accumulation of reactive oxygen species and lipid peroxide. Mechanistically, CGRP alleviates H/R-induced mitochondrial dynamics imbalance, improving mitochondrial morphology and membrane potential. In addition, CGRP inhibited abnormal expression of key proteins (IP3R, GRP75, and VDAC) at mitochondrial endoplasmic reticulum contact sites (MAMs) and reduced ferroptosis signaling. In vivo experiments demonstrated that nitroglycerin and cinnamaldehyde, a TRPA1 agonist, reduced myocardial infarction size by activating the TRPA1-CGRP pathway, while blocking the CGRP receptor could counteract this protective effect. In conclusion, our study demonstrates that CGRP mitigates myocardial ferroptosis through the regulation of mitochondrial dynamics and MAMs interactions. These findings establish CGRP as a promising therapeutic target and provide a solid theoretical foundation for combating myocardial I/R injury.
    Keywords:  CGRP; Ferroptosis; Ischemia and reperfusion; MAMs; Mitochondria dynamics
    DOI:  https://doi.org/10.1016/j.intimp.2026.116839
  66. Compr Physiol. 2026 Jun;16(3): e70172
      Osteoporosis is a metabolic bone disease characterized by reduced bone mass and deterioration of bone microarchitecture, in which impaired osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) represents a central pathological mechanism. In recent years, ferroptosis, a newly recognized form of regulated cell death, has been demonstrated to play an important role in the initiation and progression of osteoporosis. Mitochondrial dysfunction can exacerbate oxidative stress and disrupt iron metabolism, thereby triggering ferroptosis in BMSCs and ultimately inhibiting osteogenic differentiation. The present study aimed to identify and validate key genes associated with mitochondrial homeostasis and osteoporosis, with a particular focus on the role of glial cell line-derived neurotrophic factor (GDNF) in regulating mitochondrial function, suppressing ferroptosis, and promoting osteogenic differentiation of BMSCs. Gene expression data from normal human bone tissues and osteoporotic bone tissues were obtained from public transcriptomic datasets in the Gene Expression Omnibus (GEO) database. Through differential expression analysis, GDNF was identified as a candidate gene. In vitro experiments demonstrated that GDNF markedly improved mitochondrial membrane potential, reduced intracellular reactive oxygen species (ROS) levels, and restored GPX4 expression, thereby promoting osteogenic differentiation of BMSCs. Furthermore, animal experiments confirmed that GDNF intervention effectively increased bone mineral density and improved trabecular microarchitecture in ovariectomized (OVX) mice. In conclusion, this study identified GDNF may suppress ferroptosis by maintaining mitochondrial homeostasis in BMSCs, thereby enhancing osteogenic differentiation and alleviating osteoporosis, providing a potential theoretical basis for molecular targeted therapy in osteoporosis.
    Keywords:  GDNF; bone marrow‐derived mesenchymal stem cells; ferroptosis; mitochondrial homeostasis; osteogenic differentiation
    DOI:  https://doi.org/10.1002/cph4.70172