bims-mistre Biomed News
on Mito stress
Issue of 2026–05–10
thirty papers selected by
Ellen Siobhan Mitchell, MitoQ



  1. Reprod Sci. 2026 May 04.
      Female fertility relies on tightly regulated mitochondrial bioenergetics to support oocyte maturation, fertilization, and early embryonic development. Beyond ATP generation, mitochondria orchestrate redox signaling, calcium homeostasis, metabolic-epigenetic coupling, and nuclear-mitochondrial communication, thereby shaping oocyte competence and ovarian longevity. Aging, obesity, metabolic stress, and genetic perturbations disrupt these regulatory networks, leading to redox imbalance, impaired oxidative phosphorylation, altered mitochondrial dynamics, and mitochondrial DNA instability. These changes compromise granulosa cell support, impair meiotic progression, and accelerate ovarian aging, contributing to female infertility disorders such as polycystic ovary syndrome. This review integrates therapeutic strategies that actively reprogram ovarian mitochondrial function rather than merely counteracting damage. Mitochondria-targeted antioxidants-including melatonin, resveratrol, N-acetylcysteine, mitochondria-directed scavengers, and coenzyme Q10 restore redox balance, stabilize mitochondrial dynamics, and enhance oocyte bioenergetics. In parallel, metabolic modulators such as metformin, dapagliflozin, and glucagon-like peptide-1 receptor agonists reprogram ovarian bioenergetics by reshaping substrate utilization, suppressing inflammatory and oxidative signaling, and improving mitochondrial efficiency within the ovary. Collectively, these interventions demonstrate that, positioning mitochondria-centered therapies as promising strategies to preserve fertility and extend the female reproductive health span.
    Keywords:  Female fertility; Mitochondria-targeted therapeutics; Mitochondrial dysfunction; Ovarian aging; mtDNA instability
    DOI:  https://doi.org/10.1007/s43032-026-02113-8
  2. J Biol Chem. 2026 May 06. pii: S0021-9258(26)02000-4. [Epub ahead of print] 113128
      Mitochondria play a major role in cellular health, yet their contribution to chronic diseases has been underestimated. Mitochondria are essential for all tissues, and a major source of ATP in high-energy-demand organs such as brain and heart being vulnerable to mitochondrial dysfunction. Failure to repair or remove damaged mitochondria contributes to aging and chronic diseases. Cells have evolved quality control mechanisms, including mitophagy to eliminate damaged mitochondria and mitobiogenesis to replenish them. The ubiquitin-proteasome system (UPS) is responsible for removing misfolded proteins, a process that is highly ATP dependent and therefore reliant on mitochondrial function. In turn, damaged mitochondria are eliminated through coordinated actions of the UPS and lysosomal degradation through mitophagy. Many neurodegenerative diseases are characterized by the presence of disease-specific protein aggregates, such as α-synuclein aggregates in Parkinson's disease and tau neurofibrillary tangles in Alzheimer's disease. These aggregates impair mitochondrial function, while dysfunctional mitochondria generate reactive oxygen species that further exacerbate proteotoxic stress, creating a pathogenic cycle. This highlights the functional interplay between mitochondria and the UPS. Recent studies have uncovered phosphorylation of ubiquitin at Serine 65 by the mitochondrial kinase PINK1 as a key signal of mitochondrial dysfunction. Phospho-Ser65-Ubiquitin (pUb) has emerged as an indicator of mitochondrial health and a potential biomarker for aging and neurodegenerative disease. However, due largely to a lack of tools, little is known about the role of pUb in cellular physiology. Here we review the current landscape of pUb biology, the phospho-ubiquitome, and its role as biomarker for mitochondrial health, and neurodegeneration.
    Keywords:  (10): mitochondria; PINK1; Parkin; aging; autophagy; biomarker; mitophagy; neurodegeneration; phospho-ubiquitin; proteasome
    DOI:  https://doi.org/10.1016/j.jbc.2026.113128
  3. Fujita Med J. 2026 May;12(2): 151-158
       Objectives: Mitochondrial dysfunction has been implicated in neurodegenerative diseases, but evidence regarding its association with cognitive performance in the general population remains limited. This study aimed to examine the association between peripheral blood mitochondrial DNA copy number (mtDNA-CN) and cognitive function in the general Japanese population.
    Methods: We conducted a cross-sectional analysis of 282 participants (134 men and 148 women) from the Yakumo Study, a population-based health examination in Hokkaido, Japan. Peripheral blood mtDNA-CN was measured by quantitative real-time PCR and categorized into tertiles. Cognitive function was assessed using the short version of the Mini-Mental State Examination (SMMSE), the Logical Memory Test (LMT), and the Digit Cancellation Test (D-CAT). Logistic regression analyses were performed to evaluate the association between mtDNA-CN levels and cognitive performance, with adjustments for relevant demographic and clinical factors.
    Results: Lower mtDNA-CN was significantly associated with poorer SMMSE scores in women and with reduced D-CAT3 performance-reflecting attention and executive function-in men. No significant associations were observed for LMT scores in either sex. These domain- and sex-specific associations remained consistent after adjustment for potential confounders.
    Conclusions: Lower mtDNA-CN was associated with poorer cognitive performance in the general Japanese population, in a cognitive domain- and sex-specific manner. mtDNA-CN thus has potential as a non-invasive biomarker for the early identification of individuals at increased risk of cognitive decline. Longitudinal studies are necessary to evaluate its predictive utility and potential application in dementia prevention strategies.
    Keywords:  Biomarker; Cognitive function; Mitochondria; Mitochondrial DNA copy number; Peripheral blood
    DOI:  https://doi.org/10.20407/fmj.2025-038
  4. medRxiv. 2026 Apr 24. pii: 2026.04.23.26351626. [Epub ahead of print]
    FinnGen
       Background: Alzheimer's disease (AD) exhibits marked sex differences. While sex hormone levels across the lifespan likely contribute to this, little remains known about their causal impact and their relation to sex-biased genetic risk for AD. We therefore sought to identify potential shared genetic architectures, as well as causal genes and relationships, between sex hormone-related traits and AD risk.
    Methods: Large-scale AD sex-stratified genome-wide association study (GWAS) results were available from case-control, proxy-based, and population-based cohorts, including the Alzheimer's Disease Genetics Consortium, Alzheimer's Disease Sequencing Project, UK Biobank, and FinnGen. Sex hormone-related trait GWAS were available for age at menarche, menopause, and voice breaking, as well as testosterone, sex hormone-binding globulin (SHBG), progesterone, follicle stimulating hormone, luteinizing hormone, and estradiol levels. Cross-trait conjunctional analyses were conducted to identify pleiotropic overlap between sex-hormone traits and AD, followed by prioritization of candidate causal sex-biased AD genes through quantitative trait locus genetic colocalization analyses. The potential regulatory impact of sex hormones on these genes was assessed through transcription factor motif analyses. Finally, sex-stratified mendelian randomization analyses were used to infer causal effects of sex hormones on AD risk.
    Results: Genome-wide pleiotropy analyses demonstrated enrichment of AD with testosterone, SHBG, and age-at-menarche traits in women. We identified 12 high-confidence pleiotropic loci, 9 of which showed stronger AD effect sizes in women (3 in men) and 8 that were novel. Genes at these loci were often causally implicated in brain tissues and enriched for promoter-associated androgen receptor transcription factor binding motifs. Mendelian randomization indicated higher bioavailable testosterone in women (OR:0.88; 95%-CI:0.82-0.96) and higher SHBG levels in men (OR:0.86; 95%-CI:0.77-0.96) were associated with lower AD risk.
    Conclusions: Our findings reveal sex-specific shared genetic architectures between AD and sex hormone-related traits and nominate related genes that may drive sex-biases in AD risk. Several of the implicated female-biased genes are relevant to phosphatidylinositol and lipid metabolism, including Fatty Acid Desaturase 2 ( FADS2 ). While we observed no causal effect of estradiol-related traits on AD risk, the protective effects of bioavailable testosterone in women and SHBG in men provide targets for sex-informed AD risk stratification and prevention strategies.
    DOI:  https://doi.org/10.64898/2026.04.23.26351626
  5. Aging Cell. 2026 May;25(5): e70530
      Vitamin K2 is a fat-soluble vitamin that has been reported to exhibit significant anti-stress activity. Anti-stress properties are considered to be closely associated with lifespan extension. Therefore, we investigated the effects of vitamin K2 on the lifespan and stress resistance of Caenorhabditis elegans, as well as the underlying mechanisms. In the present study, we found that the effects of Vitamin K2 on C. elegans are concentration-dependent. High concentrations (10 μM) of Vitamin K2 are toxic to C. elegans, whereas lower concentrations (5 μM) are beneficial. Treatment with 5 μM Vitamin K2 can extend the lifespan of C. elegans, enhance its physiological functions, protect the intestinal barrier, and reduce the accumulation of lipofuscin associated with aging. Furthermore, Vitamin K2 enhanced the stress resistance of C. elegans by maintaining mitochondrial morphology, alleviating mitochondrial stress, reducing ROS levels, and improving mitochondrial membrane potential and ATP production. Vitamin K2 activates the JNK-1/SIR-2.1/DAF-16 signaling pathway and upregulates the expression of downstream target genes such as ctl-1, ctl-2, sod-1, sod-3, and hsp-16.2. We conclude that appropriate doses of Vitamin K2 protect C. elegans from senescence by activating the JNK-1/SIR-2.1/DAF-16-mediated anti-mitochondrial oxidative stress pathway. These findings suggest that Vitamin K2 may have beneficial effects on lifespan and mitochondrial health in C. elegans, providing a basis for further investigation into its potential relevance for aging and age-related diseases in more complex model systems.
    Keywords:   Caenorhabditis elegans ; JNK/SIR‐2.1/DAF‐16 pathway; extended the lifespan; mitochondrial stress; vitamin K2
    DOI:  https://doi.org/10.1111/acel.70530
  6. bioRxiv. 2026 Apr 28. pii: 2026.04.27.721221. [Epub ahead of print]
      Coenzyme A (CoA) is an essential cofactor required for numerous metabolic reactions, yet its ability to bind and regulate proteins remains poorly defined. Using a proteomic approach, we identified malic enzyme 2 (ME2) as a CoA-binding protein. ME2 uses NAD(P) + to convert malate to pyruvate, generating NAD(P)H to support energy production and redox homeostasis. ME2 binds CoA at an allosteric site previously thought to bind NAD(P) + . Reduced CoA has minimal effect on ME2 activity, but the oxidized form, CoA disulfide, strongly activates ME2 by promoting ME2 tetramerization and a catalytically efficient closed conformation. Under oxidative stress, ME2 facilitates CoA disulfide formation, enhancing NADPH production and cellular defense against reactive oxygen species (ROS). Mice with ME2 mutation that cannot bind CoA show impaired muscle performance, elevated ROS, and mitochondrial dysfunction. These findings establish CoA as a redox-sensing cofactor, allowing cells to respond to ROS and promote mitochondrial metabolism, and expanding the function of this essential cofactor.
    DOI:  https://doi.org/10.64898/2026.04.27.721221
  7. Redox Biol. 2026 Apr 24. pii: S2213-2317(26)00189-8. [Epub ahead of print]93 104191
      As the global population ages rapidly, delaying and preventing age-related diseases have become urgent priorities in public health and biomedical research. During aging, mitochondrial dysfunction is a core molecular hallmark and a common pathogenic mechanism underlying multiple age-related disorders. Age-related mitochondrial dysfunction typically manifests as diminished metabolic capacity, impaired organelle renewal, and disrupted redox homeostasis. These factors interact to form a feedback loop constraining mitochondrial adaptability. Specifically, the interdependent decline in NAD+ availability, impaired mitochondrial biogenesis, and excessive oxidative stress render single-pathway interventions ineffective in mitigating systemic functional impairments triggered by aging. To address this complex mechanism, this review presents a novel tri-axis anti-aging model encompassing three key compounds: nicotinamide mononucleotide/nicotinamide riboside (NMN/NR), pyrroloquinoline quinone (PQQ), and l-ergothioneine (EGT). Within this framework, NMN/NR serves as a broad NAD+-dependent regulator of mitochondrial homeostasis, with its most immediate effects on metabolic activation, while PQQ and EGT may further strengthen mitochondrial remodeling and redox resilience, respectively. While each compound has distinct functional emphases, they are highly mechanistically coupled, collectively forming a closed-loop network regulating mitochondrial number, function, and homeostasis. This review synthesizes preclinical and emerging clinical evidence supporting the standalone or combined use of NMN/NR, PQQ, and EGT across various diseases. Collectively, by conceptualizing mitochondrial aging as a systemic imbalance rather than isolated molecular defects, this paper highlights a three-axis model of NMN/NR, PQQ, and EGT. This framework offers a theoretical foundation for mitochondrial-targeted anti-aging interventions while laying the groundwork for future clinical research, nutritional interventions, and the development of multi-target combination strategies.
    Keywords:  Anti-aging; Ergothioneine; Mitochondria; NMN; NR; PQQ
    DOI:  https://doi.org/10.1016/j.redox.2026.104191
  8. Front Immunol. 2026 ;17 1781434
      Idiopathic inflammatory myopathies (IIMs) are being increasingly recognized as disorders driven by profound disturbances in cellular energy metabolism rather than inflammation alone. Recent studies have highlighted mitochondrial dysfunction, oxidative stress, and metabolic reprogramming across glucose, lipid, and amino acid pathways as central mechanisms linking energy metabolism dysregulation to sustained muscle injury. Defective mitophagy, mitochondrial DNA (mtDNA) depletion, and excessive reactive oxygen species (ROS) production create a self-amplifying loop with interferon-driven inflammation, whereas abnormal glycolysis, impaired fatty acid oxidation, and dysregulated tryptophan-kynurenine metabolism further shape the immunometabolic landscape of IIMs. These metabolic shifts not only contribute to muscle weakness and tissue degeneration but are also correlated with disease severity, autoantibody profiles, and treatment resistance. Emerging therapeutic strategies, including antioxidant approaches, mitochondrion-targeted agents, metabolic modulators, and exercise-based interventions, underscore the translational potential of targeting energy homeostasis. This review synthesizes current evidence on energy metabolism abnormalities in IIMs, integrates molecular findings with clinical implications, and highlights future directions for immunometabolic-based precision therapies.
    Keywords:  energy metabolism; idiopathic inflammatory myopathies; immunometabolism; metabolic reprogramming; mitochondrial dysfunction; oxidative stress
    DOI:  https://doi.org/10.3389/fimmu.2026.1781434
  9. Burns Trauma. 2026 ;14 tkag008
      As cellular energy metabolic hubs, mitochondria undergo dynamic fusion-fission cycles and autophagy that enable rapid adaptation to cellular energy demands and stress conditions. In addition to their role in energy metabolism, mitochondria are integral to cellular homeostasis and regulate cell cycle progression, differentiation, and apoptosis pathways. In recent years, the importance of mitochondrial function in skin health and disease has garnered increasing attention. Mitochondrial dysfunction has been implicated in a spectrum of skin disorders, including skin aging, psoriasis, vitiligo, keloids, scleroderma, and skin cancer. The pathogenesis of these conditions is closely linked to mitochondrial deoxyribonucleic acid (mtDNA) damage, excessive reactive oxygen species (ROS) production, and alterations in mitochondrial metabolic pathways. In terms of therapeutic strategies, this review summarizes a range of mitochondrion-targeted interventions. These treatments include the activation of the PGC-1α pathway to increase mitochondrial adenosine triphosphate synthesis, the use of antioxidants to mitigate mitochondrial ROS production, and the application of bioactive compounds and drugs to protect mitochondria or promote mtDNA repair. These approaches not only contribute to improved skin health but also provide novel insights for the treatment of skin diseases. Additionally, mitochondrial transplantation technology has shown considerable promise in skin regeneration and wound healing and is emerging as a new frontier for skin tissue repair.
    Keywords:  Diseases; Dynamics; Energy; Health; Mitochondrial; Skin
    DOI:  https://doi.org/10.1093/burnst/tkag008
  10. Free Radic Biol Med. 2026 May 06. pii: S0891-5849(26)00745-8. [Epub ahead of print]
      Doxorubicin is an effective chemotherapeutic agent; however, its use is limited by cardiotoxicity. Mitochondrial dysfunction is a central driver of doxorubicin-mediated cardiotoxicity. The role of the integrated stress response (ISR), a mitochondria-to-nucleus signaling pathway and crucial cellular defense mechanism in doxorubicin-induced cardiotoxicity, remains unclear. We investigated the pharmacological ISR activator salubrinal, a selective inhibitor of eukaryotic initiation factor 2α dephosphorylation with potential cardioprotective properties, to elucidate the molecular mechanisms underlying ISR-mediated cardioprotection in H9c2 cardiomyocytes, C57BL/6 mice, and HL-1 cell models. Doxorubicin disrupts ISR signaling, whereas salubrinal alleviates cardiotoxicity by activating transcription factor 4 (ATF4, a central ISR hub)-dependent pathways that suppress doxorubicin-induced apoptosis and preserve mitochondrial metabolism. The cystine/glutamate antiporter xCT, essential for glutathione (GSH) homeostasis, and growth differentiation factor 15 (GDF15), a mitochondrial stress-induced mitokine and potential biomarker of doxorubicin cardiotoxicity, are both regulated by ATF4. Mechanistically, we found that salubrinal contributes to cardioprotection against doxorubicin by enhancing the GSH-based antioxidant capacity via the ATF4-dependent GDF15-xCT axis. Further analysis of ATF4-associated GSH regulatory pathways revealed that enzymes involved in serine metabolism and glutathione peroxidase 4, a critical enzyme in GSH utilization that is upregulated by ATF4-mediated heat shock 70 kDa protein 5 and cystathionine gamma-lyase, contribute to the cardioprotective effects of salubrinal against doxorubicin-induced oxidative stress. Our findings highlight the ISR as a vital survival mechanism in cardiomyocytes exposed to doxorubicin. Regulating antioxidant defenses through enhanced GSH homeostasis and ISR activation, particularly via pharmacological agents such as salubrinal, may offer a promising therapeutic strategy for mitigating doxorubicin-induced cardiotoxicity.
    Keywords:  cardiotoxicity; doxorubicin; glutathione; integrated stress response; mitochondria; salubrinal
    DOI:  https://doi.org/10.1016/j.freeradbiomed.2026.05.281
  11. Antioxidants (Basel). 2026 Apr 01. pii: 441. [Epub ahead of print]15(4):
      N-Lactoyl-phenylalanine (Lac-Phe), identified in 2022 as an exercise-inducible signaling metabolite, is formed by carnosine dipeptidase 2 via conjugation of lactate and phenylalanine. Its circulating levels rise sharply after intense exercise in mice, humans, and racehorses, reflecting increased glycolytic flux. Beyond exercise, Lac-Phe also rises with feeding and metformin, positioning it as a potential integrator of energy intake, expenditure, and metabolic homeostasis. Centrally, Lac-Phe may contribute to appetite suppression by inhibiting hypothalamic orexigenic agouti-related protein neurons, primarily observed in obese rodent models, while sparing anorexigenic pro-opiomelanocortin neurons, thereby reducing food intake, promoting weight loss, and improving glucose tolerance in obese models without altering energy expenditure. Peripherally, it drives anti-inflammatory M2 macrophage polarization, ameliorating colitis and aiding recovery after spinal cord injury via NF-κB suppression and reactive oxygen species reduction. As a biomarker, Lac-Phe may offer advantages over lactate in reflecting mitochondrial dysfunction in conditions such as MELAS, sepsis, and NADH-reductive stress; however, these observations derive mainly from small-scale or exploratory studies and require prospective validation. Recent studies from 2024 to 2025 further reveal its partial and context-dependent role in mediating metformin's effects, intensity- and sex-dependent responses, renal clearance via SLC17A1/3 transporters, and links to exercise-induced redox adaptations. The first human phase I trial (NCT06743009), launched in 2025, is assessing the metabolic effects of Lac-Phe in obesity. This Perspective summarizes Lac-Phe biosynthesis, physiological mechanisms, including its emerging but largely correlative connections to redox homeostasis, and therapeutic promise, underscoring its potential relevance for exercise-mimicking strategies in metabolic, inflammatory, and redox-related disorders.
    Keywords:  N-lactoyl-phenylalanine; appetite suppression; exerkine; metformin; mitochondrial dysfunction; obesity; oxidative stress; redox homeostasis
    DOI:  https://doi.org/10.3390/antiox15040441
  12. Diabetes Res Clin Pract. 2026 May 01. pii: S0168-8227(26)00210-X. [Epub ahead of print] 113290
      This study evaluated whether oral melatonin supplementation influences glycemic outcomes in humans through a systematic review and meta-analysis of randomized controlled trials (RCTs). A systematic search of major electronic databases was conducted to identify RCTs evaluating the effects of melatonin supplementation on metabolic outcomes in adults. Studies reporting fasting glucose, glycated hemoglobin (HbA1c), fasting insulin, or homeostatic model assessment of insulin resistance (HOMA-IR) were included. Data were pooled using a random-effects model. Heterogeneity was assessed using the I2 statistic, and meta-regression analyses were performed to explore potential moderators. Statistical analyses were conducted using Jamovi software. Thirty-one RCTs were included in this systematic review. Quantitative synthesis comprised 27 studies reporting fasting glucose, nine studies reporting HbA1c, seven studies reporting fasting insulin, and four studies reporting HOMA-IR. Melatonin doses ranged from 1 to 10 mg/day, with intervention durations between 14 and 365 days. The meta-analysis showed no significant reduction in fasting glucose levels. However, improvements were observed in secondary metabolic outcomes related to glycemic control and insulin resistance, including HbA1c, fasting insulin, and HOMA-IR. Melatonin supplementation did not significantly reduce fasting glucose but may improve markers of glycemic control and insulin sensitivity, suggesting a modulatory role in metabolic regulation.
    Keywords:  Glycated hemoglobin; HOMA-IR; Insulin; Melatonin; Supplementation
    DOI:  https://doi.org/10.1016/j.diabres.2026.113290
  13. Healthcare (Basel). 2026 Apr 17. pii: 1080. [Epub ahead of print]14(8):
      Background/Objectives: Masters athletes are adults aged ≥40 who compete in sport, exhibiting superior physical function and healthier aging than their sedentary peers. However, even highly trained masters athletes experience age-related performance declines. Women masters athletes represent a growing yet understudied population who may face unique physiological challenges. This scoping review synthesizes literature from 1984 to 2024, examining the impact of age and menopause on determinants of endurance performance in women masters athletes. Methods: Following JBI scoping review methodology, six databases were searched (Medline, Embase, Central, CINAHL, SPORTdiscus, Scopus). Studies were evaluated for population characteristics, methodological approaches, and physiological determinants of performance (i.e., aerobic capacity, lactate kinetics, and exercise economy). Results: Twenty-nine studies were included. Most (n = 28) assessed aerobic capacity, reporting declines between 0.36 and 0.84 mL·kg-1·min-1·year-1 (0.5-2.4%·year-1). These reductions were primarily associated with decreased cardiac output followed by changes in body composition. Training volume emerged as a predictor of aerobic capacity, but the effects of menopause were unclear. Findings on lactate kinetics and exercise economy were mixed but preliminary research indicated that lactate threshold relative to VO2max generally increased, peak lactate remained stable and energy cost increased with age. Fitness and health characteristics among women athletes differed from sedentary populations, emphasizing the need for athlete-specific data to support training and health decisions. Conclusions: Aging is associated with decreased aerobic capacity and variable changes in lactate kinetics and exercise economy. While training volume may attenuate performance decrements, the impact of menopause remains uncertain, underscoring the need for longitudinal research to better support this growing segment of the population.
    Keywords:  aerobic capacity; age-related decline; economy; endurance sport; lactate; masters athlete; menopause; sport performance; women
    DOI:  https://doi.org/10.3390/healthcare14081080
  14. Chem Biol Interact. 2026 May 05. pii: S0009-2797(26)00231-0. [Epub ahead of print] 112123
      Pyrrolidinophenones (PPs), a class of synthetic cathinones, have emerged as hazardous new psychoactive substances due to their high lipophilicity and potent neurotoxicity. However, the mechanisms underlying PPs-induced neuronal damage, particularly the roles of mitochondrial reactive oxygen species (ROS) and mitophagy, remain unclear. In this study, we investigated the interplay among ROS overproduction, mitochondrial dysfunction, mitophagy, and apoptosis in human neuronal cells exposed to representative PPs. Treatment with PPs induced neuronal cell toxicity in a manner dependent on the elongation of the alkyl chain, with α-pyrrolidinooctanophenone (POP) exhibiting the strongest effects. The treatment also facilitated the production of intracellular and mitochondrial ROS, including superoxide, hydrogen peroxide, and hydroxyl radical. Furthermore, the cytotoxicity was remarkably attenuated by pretreating with antioxidant, N-acetyl-L-cysteine, indicating a critical role of ROS in PPs-induced cytotoxicity. Subcellular fractionation analysis revealed an accumulation of highly lipophilic PPs such as α-pyrrolidinoheptanophenone (PHPP) and POP in mitochondria, and the treatment with PHPP or POP resulted in an increase in Bax/Bcl2 ratio, caspase-9 activation, and mitochondrial lipid peroxidation, presumably due to an activation of mitochondria-dependent apoptotic signaling. Notably, POP induced mitophagy via activation of the PINK1/Parkin pathway. Additionally, pharmacological inhibition of autophagy or mitophagy exacerbated both ROS production and cytotoxicity, suggesting a protective role of mitophagy through the removal of damaged mitochondria. Collectively, these findings demonstrate that mitochondrial accumulation of PPs promotes ROS-dependent apoptosis, while mitophagy functions as an adaptive cytoprotective mechanism. This study provides new insights into mitochondrial quality control in PPs-induced neurotoxicity and highlights mitophagy as a potential therapeutic target.
    Keywords:  Apoptosis; Mitophagy; Neuronal SK-N-SH cell; Pyrrolidinophenones; Reactive oxygen species
    DOI:  https://doi.org/10.1016/j.cbi.2026.112123
  15. J Psychosom Obstet Gynaecol. 2026 Dec 31. 47(1): 2666107
       BACKGROUND: Estrogen fluctuations during menopause are linked to increased psychiatric symptoms like depression and anxiety. Depression rates in menopausal women are 2-3 times higher than in premenopausal women, primarily due to rapid estrogen changes. Estrogen affects emotional stability by regulating neurotransmitters, adjusting HPA axis sensitivity, and influencing neuroinflammatory and epigenetic pathways. Menopausal hormone therapy (MHT) is a key treatment, stabilizing neurotransmitter systems and HPA axis activity, but requires personalized and evidence-based approaches.
    OBJECTIVE: This paper aims to systematically summarize the association between estrogen fluctuations and menopausal psychiatric symptoms, elucidate the underlying physiological and molecular mechanisms driving these symptoms, and evaluate the therapeutic potential of MHT, so as to provide a robust theoretical basis for clinical decision-making in menopausal mental health management.
    METHODS: We performed a thorough review of peer-reviewed studies from medical and psychiatric databases, examining the connections between menopausal estrogen changes, neurotransmitter regulation, HPA axis function, neuroinflammation, epigenetic changes, and the effectiveness and safety of MHT for managing psychiatric symptoms. We prioritized high-quality clinical trials, epidemiological studies, and mechanistic research to ensure reliable evidence.
    RESULTS: The review highlights that sudden estrogen changes during menopause disrupt serotonin and norepinephrine signaling, alter HPA axis activity, and trigger neuroinflammation and epigenetic changes, increasing the risk of depression and anxiety. Menopausal hormone therapy (MHT) can alleviate these symptoms by restoring neurotransmitter balance and normalizing HPA axis function. However, its effectiveness depends on factors like treatment timing, hormone type, and individual patient characteristics, including medical history and symptom severity.
    CONCLUSION: Estrogen fluctuation is a significant modifiable risk factor for psychiatric symptoms during menopause, affecting neurotransmitter, endocrine, inflammatory, and epigenetic pathways. Menopausal hormone therapy (MHT) is effective for symptom management when personalized and administered within recommended timeframes. This underscores the importance of assessing estrogen levels and psychiatric symptoms in menopausal women to optimize MHT and enhance mental health outcomes.
    Keywords:  Menopausal syndrome; depression; estrogen levels; menopausal hormone therapy; neuroinflammation
    DOI:  https://doi.org/10.1080/0167482X.2026.2666107
  16. FASEB Bioadv. 2026 May;8 e70113
      Apolipoprotein E4 (APOE4) is the strongest genetic risk factor for Alzheimer's disease (AD), yet it's unclear how this allele promotes disease. While factors like diet and sex may modify AD susceptibility in APOE4 carriers, the interaction between these factors is poorly understood. Here, we sought to determine if APOE4, sex, and diet interact to influence AD related outcomes in mice. Male and female APOE3 and APOE4 targeted replacement (TR) mice were fed a low-fat diet or high-fat diet from 4 to 8 months old. Serum neurodegenerative disease biomarkers, brain amyloid beta (Aβ), APOE, and tau, learning and memory, hippocampal mitochondrial function and proteomics data were collected. Serum GFAP and NfL were unaffected by APOE4, while HFD was associated with greater serum NfL and GFAP. Whole brain Aβ was significantly altered by sex, diet, and genotype. There was a main effect of genotype on levels of brain APOE with levels being lower in APOE4 mice. APOE4 TR mice also exhibited impaired learning before diet. Proteomic analysis revealed that APOE4 exerts diet- and sex-dependent effects on mitochondrial pathways. This included downregulation of pyruvate metabolism in HFD males and oxidative phosphorylation in HFD females. Basal respiration was lower in APOE4 versus APOE3 TR females. We provide novel evidence that APOE4 may drive early sex- and diet-dependent reductions in pathways that support brain mitochondrial energy metabolism.
    Keywords:  Alzheimer's disease; apolipoprotein E; learning; memory; mitochondria; neurodegeneration
    DOI:  https://doi.org/10.1096/fba.2026-00121
  17. Menopause. 2026 May 05.
       IMPORTANCE AND OBJECTIVE: Aging is a complex biological process uniquely shaped in women by hormonal transitions, particularly across the menopause transition. While chronological age alone fails to capture individual health variability, emerging molecular biomarkers offer tools to quantify biological aging and understand mechanisms underlying age-related decline. This review synthesizes the current landscape of aging biomarkers, including senescence-associated secretory phenotype factors, epigenetic clocks, clonal hematopoiesis of indeterminate potential, and telomere length, with a particular emphasis on their relevance to menopause.
    METHODS: This narrative review synthesizes human studies, translational research, and foundational basic science identified through PubMed searches through June 2025, examining aging biomarkers in general populations, among women in the menopause transition, and in relation to vasomotor symptoms and hormone therapy.
    DISCUSSION AND CONCLUSION: Evidence demonstrates that changes in biological aging biomarkers are observed across multiple molecular systems during midlife, including the menopause transition, reflecting broader age-related biological remodeling. Postmenopausal status, particularly following early or surgical menopause, has been associated with biological aging phenotypes, including elevated senescence-associated secretory phenotype factors, epigenetic age acceleration, clonal hematopoiesis, and shorter leukocyte telomere length, likely reflecting a combination of chronological aging, hormonal changes, and individual biological vulnerability. While severe vasomotor symptoms have been linked to higher epigenetic age, hormone therapy may favorably influence certain senescence markers and biological age discrepancy. Despite these advances, significant limitations constrain clinical translation, as current biomarkers capture overlapping biological processes and lack validated thresholds to define biological aging, especially in women. Future research requires large, longitudinal studies across diverse populations to establish clinically meaningful thresholds and sex-specific calibration. Advancing precision health strategies for women requires a better understanding of how reproductive and hormonal factors modify biomarker trajectories to improve risk prediction and to facilitate the development of targeted interventions for age-related diseases.
    Keywords:  Biological aging; Cellular senescence; Epigenetic clocks; Hormone therapy; Menopause; Telomere length
    DOI:  https://doi.org/10.1097/GME.0000000000002802
  18. medRxiv. 2026 Apr 24. pii: 2026.04.23.26351500. [Epub ahead of print]
      Earlier menopause is a risk factor for several age-related diseases, including dementia. The biological pathways linking menopause timing to later-life brain aging are not understood. Leveraging large-scale plasma proteomics in postmenopausal women from the UK Biobank ( N =15,012), earlier menopause was associated with upregulation of pro-inflammatory and extracellular matrix degradation pathways, plus accelerated aging across proteomic clocks of organ and cellular aging, including brain and oligodendrocyte aging. Elevated GDF15, a canonical aging marker, was the top protein correlate of earlier menopause. We observed robust replication of menopause timing proteomic shifts in the Women's Health Initiative Long Life Study ( N =1,210). In UKB, proteins associated with earlier menopause, including GDF15, exhibited concordant associations with incident dementia risk and brain atrophy, cerebral small vessel disease burden, and white matter microstructural integrity. Collectively, our findings identify proteomic signatures linking ovarian aging to brain aging, providing a framework to inform interventions to reduce dementia risk.
    DOI:  https://doi.org/10.64898/2026.04.23.26351500
  19. iScience. 2026 May 15. 29(5): 115555
      Diabetic nephropathy (DN) involves mitochondrial dysfunction, but the role of complex I subunit NDUFA5 is unclear. This study investigated its protective mechanisms. Using tubule-specific Ndufa5 knockout mice, streptozotocin-induced diabetic mice, and high glucose-treated human kidney-2 (HK-2) cells, we assessed the effects of NDUFA5 manipulation. Renal NDUFA5 expression was reduced in diabetes. Its knockout exacerbated mitochondrial damage, ROS overproduction, and renal injury, while AAV9-mediated overexpression ameliorated these defects. NDUFA5 overexpression also suppressed pro-inflammatory cytokines (interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), and monocyte chemoattractant protein-1 (MCP-1)) and nuclear factor-κB (NF-κB) signaling in vivo and in vitro. Mechanistically, NDUFA5 attenuated inflammation by inhibiting mitochondrial reactive oxygen species (mtROS) generation. Thus, NDUFA5 protects against DN, at least in part, by preserving mitochondrial integrity and reducing oxidative stress and inflammation, highlighting its potential as a therapeutic target.
    Keywords:  biological sciences; functional aspects of cell biology; health sciences; molecular biology
    DOI:  https://doi.org/10.1016/j.isci.2026.115555
  20. J Physiol. 2026 May 07.
      
    Keywords:  cytoskeleton; mitochondrial dynamics; mitochondrial function; skeletal muscle metabolism
    DOI:  https://doi.org/10.1113/JP291379
  21. Molecules. 2026 Apr 11. pii: 1262. [Epub ahead of print]31(8):
      Ultraviolet A (UVA) radiation induces oxidative stress and mitochondrial dysfunction in dermal fibroblasts, contributing to photodamage and skin aging. This study investigated the protective effects of Yeast/rice fermentation filtrate (RFF) and sialic acid (SA), both individually and in combination, against UVA-induced damage in human dermal fibroblasts. Cell viability, reactive oxygen species (ROS) levels, intracellular ATP and NAD+ contents, and mitochondrial membrane potential (ΔΨm) were evaluated following treatment. RFF, SA, and their combination significantly improved cell viability in UVA-damaged fibroblasts and reduced ROS generation. Notably, the combined treatment increased intracellular ATP levels by 201.2% (p < 0.05), with enhancements of 62.3% and 285.4% compared to RFF and SA alone, respectively. Additionally, the combined treatment significantly restored NAD+ levels and effectively preserved mitochondrial membrane potential. Transcriptomic analysis revealed modulation of pathways related to cellular energy metabolism, particularly AMPK, and upregulation of SIRT1, SIRT3, and SIRT5 expression. The RFF-SA combination confers robust UVA photoprotection by enhancing mitochondrial resilience, providing a foundation for the development of protective cosmetic formulations.
    Keywords:  UVA-induced oxidative stress; dermal fibroblasts; mitochondrial protection; photoprotection; sialic acid; yeast/rice fermentation filtrate
    DOI:  https://doi.org/10.3390/molecules31081262
  22. Bioorg Chem. 2026 Apr 26. pii: S0045-2068(26)00461-X. [Epub ahead of print]177 109925
      Mitohormesis, an adaptive cellular response to moderate mitochondrial stress, represents a promising therapeutic paradigm. To pharmacologically harness this phenomenon, we developed mitochondrial respiration inhibitors by conjugating a thiazole-based pharmacophore to a triphenylphosphonium (TPP) cation. Here, we report three TPP-thiazole conjugates which are distinguished by their hydrolytically labile linkers, comprising an ester (Compound 1), a more labile thioester (Compound 2), and a more stable amide (Compound 3). In vitro evaluation demonstrated that the hydrolytic stability of the linkers correlated inversely with inhibitory potency, where Compound 2 exhibited the strongest inhibition, followed by Compound 1. In contrast, Compound 3 showed negligible activity, lacking a clear dose-response relationship. As therapeutic mitohormesis requires a mild stress induction within a beneficial hormetic window, Compound 1 was selected for further investigation based on its intermediate inhibition and pronounced biphasic effects. Compound 1 activated the mitochondrial unfolded protein response (UPRmt) in Caenorhabditis elegans (C. elegans) and stimulated transcription of mitokines in both C. elegans and mice. In a murine model of diet-induced type 2 diabetes, Compound 1 significantly improved systemic metabolism, ameliorating glucose intolerance, insulin resistance, and hepatic steatosis. Furthermore, it outperformed metformin at an equivalent dose without observed toxicity. Collectively, these findings establish the rationally tuned inhibition of mitochondria as a viable small-molecule strategy for the treatment of metabolic disorders through mitohormesis.
    Keywords:  Metabolic disorders; Mitochondria; Mitohormesis; TPP-thiazole; UPR(mt)
    DOI:  https://doi.org/10.1016/j.bioorg.2026.109925
  23. Nutrients. 2026 Apr 10. pii: 1192. [Epub ahead of print]18(8):
      Background/Objectives: Creatine is a supplement that, beyond its physiological effects, has been shown to have positive effects on cognitive abilities. In our previous study, we showed that a single dose of 0.35 g/kg creatine induces changes in brain metabolism during sleep deprivation and reduces deterioration in cognitive performance. The present study investigates whether supplementation of a lower dose is associated with cognitive effects during sleep deprivation, focusing exclusively on cognitive performance outcomes. Methods: Twenty-nine healthy subjects performed cognitive tests at the evening baseline and 3, 5.5, and 7.5 h after receiving a single dose of creatine monohydrate (0.2 g/kg) or a placebo during a total of 21 h of sleep deprivation (SD). Results: The results show a mitigating effect of creatine on sleep deprivation-induced deterioration in logical and numerical tasks, language-related processing speed, and the Psychomotor Vigilance Test (PVT). Compared to males, females benefit more in logic, PVT and processing speed in language and logic tasks. Conclusions: Our results show that a dose of 0.2 g/kg creatine is associated with a reduced deterioration in cognitive performance during sleep deprivation. Although the effect is less pronounced than with a high dose of 0.35 g/kg, there is still an improvement of up to 12%.
    Keywords:  cognitive performance; creatine; sleep deprivation
    DOI:  https://doi.org/10.3390/nu18081192
  24. Drug Des Devel Ther. 2026 ;20 560034
      Fibroblast growth factor 21 (FGF21) is an endocrine hepatokine that coordinates systemic energy metabolism by linking hepatic nutrient sensing with adipose and central signalling pathways. Experimental and clinical studies identify FGF21 as a critical modulator of lipid oxidation, insulin sensitivity, and inflammatory balance, processes central to the pathogenesis of metabolic dysfunction-associated steatohepatitis (MASH). Endogenous FGF21 rises in response to fasting, lipotoxicity, and mitochondrial stress, yet this compensatory increase is insufficient in chronic metabolic disease, reflecting target-tissue resistance. Pharmacologic augmentation with engineered FGF21 analogues demonstrates robust reductions in hepatic fat, serum transaminases, and fibrosis biomarkers, along with improvements in triglyceride and adiponectin levels as well as liver histology. In a Phase 2b trial, efruxifermin reversed cirrhosis in 39% of participants. These agents act across the MASH cascade, mitigating lipotoxic injury, inflammation, and stellate-cell activation while favorably modifying cardiometabolic risk. FGF21 therefore represents a unifying therapeutic axis that integrates hepatic and systemic metabolic correction. Ongoing Phase 3 studies will determine whether these biochemical and histologic improvements translate into long-term clinical benefit, positioning FGF21 analogues as cornerstone therapies for metabolic disease. This review aims to synthesize current evidence on the molecular mechanisms and therapeutic potential of FGF21 in metabolic dysfunction-associated steatohepatitis. It highlights emerging clinical data on FGF21 analogues and their role in targeting key pathways of disease progression, with implications for future therapeutic strategies.
    Keywords:  MASH; MASLD; cardiometabolic disease; efruxifermin; fibroblast growth factor 21; hepatic fibrosis; insulin resistance
    DOI:  https://doi.org/10.2147/DDDT.S560034
  25. Int J Mol Sci. 2026 Apr 09. pii: 3386. [Epub ahead of print]27(8):
      Chronic social isolation (CSIS) is a form of psychosocial stressor strongly associated with the development of depression. Preclinical studies demonstrated that CSIS induces behavioral phenotypes resembling human depression, including anhedonia, behavioral despair and anxiety. This review summarizes proteomic-driven discoveries characterizing hippocampal non-synaptic mitochondria (NSM) and synaptosomal fractions containing synaptic mitochondria from adult male rats exposed to six weeks of CSIS, an animal model of depression, compared to controls. The compartment-specific proteomic alterations reveal mechanisms underlying mitochondrial dysregulation, providing molecular insights into the depression-like phenotype. Hippocampal NSM exhibit changes in energy metabolism-related proteins, including components of the tricarboxylic acid cycle and oxidative phosphorylation, as well as mitochondrial transport proteins and alterations in chaperones, structural and translational proteins, and monoamine oxidase, further elucidating how these proteomic changes contribute to mitochondrial dysregulation. In contrast, synaptosomal proteomics reveal predominantly increased protein abundance associated with energy metabolism, signaling, cytoskeletal organization, protein quality control, and vesicle trafficking, suggesting compensatory adaptations. Together, these findings highlight compartment-specific mitochondrial proteomic changes that may underlie depression-like behaviors and represent potential targets for therapeutic intervention.
    Keywords:  depression-like behaviors; hippocampus; non-synaptic mitochondria; proteomics; synaptosomes
    DOI:  https://doi.org/10.3390/ijms27083386
  26. Food Sci Nutr. 2026 May;14(5): e71826
      Protocatechuic acid (PCA), a natural phenolic compound with antioxidant and anti-inflammatory properties, has been proposed as a potential therapeutic agent against aging-related diseases. This study investigated the protective effects of PCA on D-galactose (D-gal)-induced renal aging in mice. PCA administration significantly improved renal function, alleviated oxidative stress and inflammatory responses, and ameliorated histopathological abnormalities. Biochemical analyses revealed reductions in serum AGEs, β-galactosidase, creatinine, and blood urea nitrogen, accompanied by restoration of antioxidant enzyme activities and suppression of proinflammatory cytokines. Transcriptomic and metabolomic profiling further demonstrated that PCA reversed D-gal-induced molecular alterations, with integrated multi-omics analysis identifying taurine and hypotaurine metabolism as the key pathway mediating its renoprotective effects. Western blot validation confirmed that PCA regulates CSAD, an enzyme essential for taurine biosynthesis. Collectively, these findings provide novel mechanistic insights into renal aging and highlight PCA as a promising natural agent for delaying kidney senescence through modulation of taurine metabolism.
    Keywords:  D‐galactose; oxidative stress; protocatechuic acid; renal aging; taurine metabolism
    DOI:  https://doi.org/10.1002/fsn3.71826
  27. Biogerontology. 2026 May 04. pii: 96. [Epub ahead of print]27(3):
      Aging, stress-related disorders, and chronic disease are often examined across separate domains-stress physiology, nutrition, psychiatry, and geroscience-despite converging on shared phenotypes of functional decline and reduced resilience. Although adaptive responses to stress are well characterized, why comparable exposures yield sustained resilience in some individuals but progressive dysfunction in others remains insufficiently explained. We propose that the missing unifying constraint is not stress exposure itself, but the bioenergetic capacity to complete recovery. We reframe stress adaptation as a cyclical process comprising response, adaptation, and recovery, emphasizing that recovery is an active, ATP-dependent phase conditionally funded within a finite bioenergetic system. When mitochondrial processing capacity and redox flexibility are constrained, adaptive programs may persist beyond their functional window, contributing to mitochondrial congestion, epigenetic gridlock, and progressive loss of physiological plasticity-even in the absence of overt pathology. Within this perspective, we introduce Exposure-Related Malnutrition (ERM) as a proposed conceptual model describing a clinically interpretable and potentially reversible phenotype of unresolved bioenergetic triage. ERM is proposed to describe a state of relative undernutrition arising from chronic mismatch between energetic demand and recovery capacity, often occurring despite nominal intake and laboratory values within reference ranges. Distinct from frailty, sarcopenia, cachexia, metabolic syndrome, and classical malnutrition, ERM may reflect an upstream constraint in ATP-dependent recovery rather than structural loss, inflammatory wasting, metabolic thresholds, or inadequate intake. By integrating evolutionary allocation theory, developmental calibration, stress physiology, and mitochondrial mechanics, ERM is proposed to offer a unifying integrative framework for functional decline across aging and chronic disease. Clinically, this perspective shifts risk assessment from isolated thresholds toward coordinated biomarker patterns, trajectories, and recovery kinetics, potentially enabling recognition of vulnerability before incomplete resolution consolidates into irreversible pathology. We further outline translational implications of a recovery-centered approach, positioning mitochondrial processing capacity and intercellular bioenergetic support as modifiable determinants of long-term resilience.
    Keywords:  Aging and chronic disease; Bioenergetic resilience; Exposure-Related Malnutrition (ERM); Mitochondrial capacity; Stress adaptation and recovery
    DOI:  https://doi.org/10.1007/s10522-026-10445-w
  28. bioRxiv. 2026 Apr 25. pii: 2026.04.23.719926. [Epub ahead of print]
      Despite increasing data demonstrating dopamine as an inflammatory mediator of the innate immune system, the molecular mechanisms underlying its effects in human cells remain incompletely defined. Here, we define an unrecognized pathway in which dopamine induces robust IL-6 secretion in primary human monocyte-derived macrophages (hMDMs) through mitochondrial stress. Dopamine initiates a transient mitochondrial membrane depolarization that leads to sustained alterations in mitochondrial dynamics, including morphology and metabolism, in a time-dependent manner. These events promote the mtDNA release into the cytoplasm, triggering cGAS-STING pathway and downstream NF-κB signaling. Pharmacological inhibition at multiple nodes of this pathway attenuates IL-6 secretion, establishing mitochondrial dysfunction and cGAS-STING signaling as central mediators of dopamine-driven IL6 secretion. Variability in dopamine receptor expression across donors correlates with the magnitude of IL-6 responses. Together, these findings redefine the interface between dopamine signaling and systemic inflammation and highlight an unrecognized source of inter-individual variation in immune responses.
    DOI:  https://doi.org/10.64898/2026.04.23.719926
  29. Biomedicines. 2026 Mar 30. pii: 783. [Epub ahead of print]14(4):
      Ubiquitin-specific protease 2 (USP2) is a deubiquitinase that controls various cellular events, including cell cycle progression and tumorigenesis. Along with cell culture models, mouse models induced using chemical blockers and gene engineering have substantially contributed to our knowledge of the crucial roles of USP2 in energy metabolism and metabolic disorders. This review summarizes the evidence of the role of USP2 in regulating energy metabolism in mice and cells under physiological and pathological conditions. In hepatocytes, a short isoform of USP2, USP2b, aggravates type 2 diabetes and metabolic dysfunction-associated steatotic liver disease. Meanwhile, a long isoform of USP2 in adipose tissue macrophages, USP2a, attenuates the onset of diabetes. USP2a mitigates insulin resistance and subsequent muscle atrophy. In ventromedial hypothalamic neurons, USP2b inhibits an increase in blood glucose by repressing hepatic glycogenolysis. In addition to regulating diabetes, USP2 isoforms potentially regulate the progression of atherosclerosis by modulating macrophages and hepatocytes. In brown adipose tissue, USP2a regulates thermogenesis, thus influencing systemic energy control. Meanwhile, in testicular macrophages, USP2 protects the mitochondrial respiration of sperm and consequently contributes to maintaining the quality of frozen sperm for use in the treatment of male infertility. As USP2 is distributed to multiple cellular components, it mediates the polyubiquitination of various molecules. For instance, USP2 modulates the stability of various transcription regulators, including C/EBP-α, PPARγ, EBF2, and PGC1α. The accumulating evidence indicates that USP2 functions as a modulatory molecule for energy metabolism across organs.
    Keywords:  MASLD; USP2; atherosclerosis; diabetes mellitus; insulin tolerance; male infertility; obesity; oncogenesis; proteasome; ubiquitination
    DOI:  https://doi.org/10.3390/biomedicines14040783
  30. Pharmacol Res. 2026 May 05. pii: S1043-6618(26)00144-1. [Epub ahead of print] 108229
      Healthy aging has become an attractive focus of biomedical research worldwide. Tryptophan (Trp) metabolism pathways that yield kynurenine, indole derivatives, and 5-hydroxytryptophan during microbiota-host crosstalk regulate molecular processes critical to healthy aging. Here, we synthesize the most recent advances concerning the mechanisms by which microbial Trp metabolism maintains homeostasis from the perspectives of improving intestinal function, modulating immune signaling, restoring redox balance, and optimizing energy production. We further evaluate the latest evidence regarding how microbiota-derived Trp metabolites influence age-related disorders. Finally, we summarize the clinical applications of Trp metabolites and key metabolic enzymes to promote healthy aging. Our review provides comprehensive insights into the relationship between microbial Trp metabolism and human aging, and it opens up novel opportunities for prevention, diagnosis, and therapy of disease.
    Keywords:  AhR pathway; gut microbiota; healthy aging; indole; tryptophan
    DOI:  https://doi.org/10.1016/j.phrs.2026.108229