bims-mihora Biomed News
on Mitohormesis, repair and aging
Issue of 2025–11–02
25 papers selected by
Lisa Patel, Istesso



  1. Physiology (Bethesda). 2025 Oct 25.
      As populations age worldwide, understanding the biology of aging and its contribution to disease becomes increasingly important. Cellular senescence, a hallmark of aging, plays a pivotal role in shaping inter-organ communication and systemic health. Once viewed primarily as a local mechanism to prevent the proliferation of damaged cells, senescence is now recognized as a dynamic, multifaceted process that influences physiology across the lifespan. Through senescence-associated secretory phenotype (SASP) proteins and other signaling modalities, including metabolites, extracellular vesicles, immune cells, and neural circuits, senescent cells contribute to both homeostatic regulation and the propagation of chronic inflammation, fibrosis, and age-related disease. These effects are often context-dependent, and senescence in one organ can influence distant tissues, driving asynchronous aging and disease vulnerability. This review examines the mechanisms by which senescent cells facilitate inter-organ communication, including emerging roles for blood-borne factors, immune cell dynamics, and neuroendocrine signals. We highlight illustrative examples of organ crosstalk and emphasize the potential translational relevance of these pathways. We also examine therapeutic strategies aimed at modulating senescence, including senolytics, senomorphics, and interventions targeting specific SASP components, as well as the potential of lifestyle modifications to mitigate biological aging. Understanding senescence and the associated inter-organ communication offers new insights into aging biology and opens promising avenues for addressing age-related diseases in an integrated, organ-spanning framework.
    Keywords:  Aging; Cellular Senescence; SASP; Senolytics; Senomorphics
    DOI:  https://doi.org/10.1152/physiol.00017.2025
  2. Virulence. 2025 Dec;16(1): 2580132
      In response to external or endogenous stress, eukaryotic cells can activate a common adaptive pathway called the integrated stress response (ISR). The ISR reduces global protein translation but upregulates the expression of stress response proteins to either restore cellular homeostasis or, in case of severe or prolonged stress, promote cell death. The bZIP transcription factor ATF4 plays a deciding role in cellular fate upon ISR activation, but the precise mechanisms underlying such decision-making remain unclear. Although bacterial infection has previously been observed to induce the ISR, the effects of this pathway on bacterial pathogenesis and host defense are not well understood. The functions of ATF4 in this process remain even more elusive. Using the Caenorhabditis elegans model to explore the bacterial infection-induced ISR, we found that infection with Salmonella enterica induced the GCN-2/eIF-2α/ATF-4 signaling pathway to modulate host defense against the infection. More specifically, ATF-4 suppressed the expression of ribosomal protein genes in response to S. enterica exposure, reducing worm survival against the pathogen. Because ribosomal proteins are directly involved in protein translation, our data revealed an important, novel mechanism by which ATF-4 mediates the reduction of global translation under stress by inhibiting the expression of ribosomal proteins. ATF-4 also regulates components of mitochondrial electron transport and collagen genes in response to S. enterica infection; both regulations are linked to stress resistance and longevity. Overall, we have identified specific molecular mechanisms through which ATF-4 determines cell fate upon ISR activation, revealing how this pathway influences host outcomes during bacterial infection.
    Keywords:  ATF-4; C. elegans; GCN-2/eIF-2α/ATF-4 signaling pathway; Host-pathogen interactions; Salmonella enterica; host response to infection; integrated stress response; ribosomal proteins; stress resistance; stress response
    DOI:  https://doi.org/10.1080/21505594.2025.2580132
  3. Genes Dev. 2025 Oct 29.
      Mitochondria play a crucial role in cellular energy metabolism and homeostasis and are strongly implicated in aging and age-related diseases. The outer mitochondrial membrane protein voltage-dependent anion channel (VDAC) plays multiple roles in mitochondrial homeostasis, including transport of metabolites, ATP, and Ca2+ Dysregulation of VDAC levels has been associated with cancer, neurodegeneration, metabolic disorders, and aging. Previously, we demonstrated that elevated VDAC-1 levels in Caenorhabditis elegans lead to increased mitochondrial permeability and reduced life span. Here we demonstrate that reduced VDAC-1 function extends life span through the activation of the mitochondrial unfolded protein response (UPRmt), a conserved stress response that maintains mitochondrial proteostasis and is linked to life span extension in multiple species. Leveraging unbiased genomic discovery, we identified genes encoding several proteins in the PeBoW complex as a critical mediator of UPRmt activation following VDAC-1 loss. More broadly, we demonstrated a universal requirement for several PeBoW component genes across diverse mitochondrial stressors in order to fully animate the UPRmt Our findings reveal a heretofore unappreciated role for PeBoW components in UPRmt induction and life span extension in response to mitochondrial stress, highlighting its essential function in mitochondrial quality control and longevity pathways.
    Keywords:  PeBoW; mito-stress; mitoUPR; mitochondria
    DOI:  https://doi.org/10.1101/gad.352979.125
  4. Biochem Biophys Res Commun. 2025 Oct 28. pii: S0006-291X(25)01597-9. [Epub ahead of print]789 152881
      Cellular senescence is emerging as one of the leading underlying mechanisms of ageing. Senescent cells are observed in most tissues and organs with advancing age, which augments tissue dysfunction and inflammatory disorders. Extracellular vesicles (EVs) are nanoscale sacs released by almost all cells, which carry cell-type dependent molecular cargo that can exhibit pharmacological effects in recipient cells. Since senescence represents a global phenomenon in an organism, and EVs are released by various cell types, this review attempts to delineate their intricate interactions in regulating various facets of cellular senescence and age-related diseases, as well as potential diagnostic avenues, research gaps, and challenges. EVs released by senescent cells are biophysically different and can not only promote bystander senescence in healthier cells but can also accelerate the development of age-dependent chronic disorders by promoting a pro-tumorigenic and pro-inflammatory environment. Conversely, EVs isolated from healthy cells, typically stem cells, can suppress senescence, promote inflammatory homeostasis, and improve lifespan in vivo. Novel non-mammalian sources of EVs, including the gut microbiota and dietary plants, are also being recognised with potentially senescence-modulatory effects. A previously unknown role of EVs in modulating immune cell response during senescence is also developing, and EVs-based biomarkers are identified with the aim of early prediction and diagnosis of senescence. However, several challenges remain at the technical and translational end of EVs, and future research should focus on the identification of EVs in senescent cell subtypes and immune cells, understanding non-mammalian sources of EVs in modulating senescence, and establishing the safety of EVs to fully comprehend their pathological, therapeutic, and diagnostic potential in regulating cellular senescence.
    Keywords:  Ageing; Cellular senescence; Exosomes; Extracellular vesicles; Mesenchymal stem cells; Senescent cells
    DOI:  https://doi.org/10.1016/j.bbrc.2025.152881
  5. Life (Basel). 2025 Sep 23. pii: 1498. [Epub ahead of print]15(10):
      Aging is accompanied by complex cellular and molecular changes that compromise CNS function. Among these, glial cells (astrocytes, microglia, and oligodendrocytes) play a central role in maintaining neural homeostasis, modulating synaptic activity, and supporting metabolic demands. Emerging evidence indicates that aging disrupts glial cell physiology through processes including mitochondrial dysfunction, impaired proteostasis, chronic low-grade inflammation, and altered intercellular signaling. These alterations contribute to synaptic decline, myelin degeneration, and persistent, low-grade inflammation of the CNS. This review synthesizes current knowledge on the bidirectional relationship between aging and glial cell dysfunction, highlighting how age-related systemic and CNS-specific factors exacerbate glial impairments and, in turn, accelerate neural deterioration. Finally, this study discusses some potential therapeutic strategies aimed at preserving or restoring glial function to promote CNS resilience in aging populations. Understanding this interplay offers critical opportunities for mitigating cognitive decline and improving quality of life in older adults.
    Keywords:  aging; astrocytes; glial cells; inflammaging; microglia; neuroinflammation; oligodendrocytes; senescence
    DOI:  https://doi.org/10.3390/life15101498
  6. Biomolecules. 2025 Sep 24. pii: 1354. [Epub ahead of print]15(10):
      Mitochondria possess their own genome, which encodes subunits of the electron transport chain, rendering mitochondrial protein translation essential for cellular energy metabolism. Mitochondrial dysfunction affects nuclear transcription through the retrograde response. We applied RNA-seq to investigate whether and how the inhibition of mitochondrial translation by chloramphenicol (CAP) affects transcriptome regulation in proliferating or stationary-phase cells of Schizosaccharomyces pombe growing in fermentative or respiratory media. Stationary-phase cells in glucose medium exhibited the strongest transcriptome response to CAP, characterized by expression signatures similar to those observed under other stresses, including the retrograde response. The induced genes were also significantly enriched in cytoplasmic carbon metabolism pathways, reflecting a transcriptional reprogramming from respiration to fermentation. The transcription factors Scr1 and Rst2, regulators of carbon catabolite repression (CCR), controlled a common set of carbon metabolism genes in CAP-treated stationary-phase cells, and they showed opposing effects on the lifespan of these cells. Rst2 was required for the induction of carbon metabolism genes and maintained nuclear localization in CAP-treated stationary-phase cells. A systematic genetic interaction screen revealed functional relationships of Rst2 with processes related to stress and starvation responses. These findings uncover a complex transcriptional program in stationary-phase cells that adapt to inhibited mitochondrial translation, including stress- and retrograde-like responses, contributions of the CCR factors Scr1 and Rst2, and adjustment of carbon metabolism to deal with mitochondrial dysfunction.
    Keywords:  RNA-seq; S. pombe; Scr1; carbon catabolite repression; genetic interactions; mitochondrial metabolism; retrograde response; stress response; transcription factor; transcriptome
    DOI:  https://doi.org/10.3390/biom15101354
  7. Br J Pharmacol. 2025 Oct 29.
      Ageing brings about various biochemical, structural and mechanical alterations within tissues, profoundly impacting cellular behaviour and function. One of the hallmark changes observed with ageing is an increase in cellular microenvironment stiffness, a biomechanical property influenced by intrinsic factors within the cell and extrinsic factors from the surrounding extracellular matrix (ECM). This shift in ECM stiffness has been implicated in the development and progression of several age-related diseases, but the exact molecular mechanisms underlying different organ tissues remain to be fully elucidated. This review examines the lung and ovaries, two organ tissues with distinct functions but interconnected by similar timing of changes in ECM stiffness with age. We discuss common pathways and factors that drive changes in the ECM stiffness of these organs. Such insights may pave the way for innovative treatments addressing the root causes of age-related diseases, ultimately enhancing the ageing population's health span and quality of life.
    Keywords:  ECM stiffness; lung ageing; mechanopharmacology; mechanotransduction; ovarian ageing
    DOI:  https://doi.org/10.1111/bph.70236
  8. Ann Intensive Care. 2025 Oct 27. 15(1): 174
      The understanding of the response to stress in critical illness has significantly improved in recent years. These adaptations unfold across acute, subacute, and chronic phases, with an early adaptive catabolic state, marked anabolic resistance, and a later transition toward recovery. The aim of this updated review is to summarize recent advancements focusing on pathophysiological changes in endocrine, immune, gut, and mitochondrial functions and their effects on the metabolic shift in energy production, using glycolysis and the utilization of lactate and ketones as alternative pathways to meet cellular energy demands. Advances in understanding key elements such as energy expenditure and autophagy have expanded our knowledge. Furthermore, there is increased interest in the consequences of an intense and prolonged stress response, which can lead to ICU-acquired weakness (ICU AW) and post-intensive care syndrome. Recent evidence indicates that higher protein strategies generally do not improve survival or functional recovery and may signal harm in patients with renal dysfunction, supporting cautious, phase-appropriate protein dosing rather than routine high targets. New concepts, such as chronic critical illness (CCI) and persistent inflammation, immunosuppression, and catabolism syndrome (PICS), have also emerged to characterize prolonged stress responses. For glycaemic management, intensive control offers no outcome benefit and increases hypoglycaemia risk; moderate targets are preferred. Parallel advancements in monitoring techniques, such as indirect calorimetry and body composition analysis, have improved the assessment of the consequences of the metabolic changes. Metabolomics has offered deeper characterisation of the metabolic response to stress and nutrition, highlighting key metabolic pathways and potential therapeutic targets. Integrating biomarkers and metabolomics to define clinical endotypes may help time the transition from catabolic to anabolic strategies and personalize nutrition and pharmacologic support at the bedside. New therapeutic avenues have emerged or are under investigation, including glycaemic control, nutritional strategies, and some specific interventions targeting key components of the metabolic response. In this context, we present a narrative review of the literature with a focus on the clinical consequences of the pathophysiological and metabolic response to stress, alongside therapeutic implications and future perspectives.
    Keywords:  Anabolic resistance; Autophagy; Critical care; Early macronutrient restriction; Energy expenditure; Glycaemic control; Insulin sensitivity; Metabolomics; Post-intensive care syndrome
    DOI:  https://doi.org/10.1186/s13613-025-01588-z
  9. Nat Commun. 2025 Oct 28. 16(1): 9502
      Cells rapidly and extensively remodel their transcriptome in response to stress to restore homeostasis, but the underlying mechanisms are not fully understood. Here, we characterize the dynamic changes in transcriptome, epigenetics, and 3D genome organization during the integrated stress response (ISR). ISR induction triggers widespread transcriptional changes within 6 h, coinciding with increased binding of ATF4, a key transcriptional effector. Notably, ATF4 binds to hundreds of genes even under non-stress conditions, priming them for stronger activation upon stress. The transcriptional changes at ATF4-bound sites during ISR do not rely on increased H3K27 acetylation, chromatin accessibility, or rewired enhancer-promoter looping. Instead, ATF4-mediated gene activation is linked to the redistribution of CEBPγ from non-ATF4 sites to a subset of ATF4-bound regions, likely by forming an ATF4/CEBPγ heterodimer. CEBPγ preferentially targets the sites pre-occupied by ATF4, as well as genomic regions exhibiting a unique higher-order chromatin structure signature. Thus, the transcriptional responses during ISR are largely pre-wired by intrinsic chromatin properties. These findings provide critical insights into transcriptional remodeling during ISR with broader implications for other stress responses.
    DOI:  https://doi.org/10.1038/s41467-025-64577-7
  10. Mol Biol Rep. 2025 Oct 29. 53(1): 22
      Autophagy and cellular senescence are intimately linked processes that play pivotal roles in renal homeostasis, aging, and disease progression. Autophagy preserves intracellular integrity by degrading damaged organelles, misfolded proteins, and metabolic waste through lysosomal pathways, thereby maintaining energy balance and delaying senescence. However, with advancing age or persistent stress, autophagic activity declines, leading to the accumulation of senescent cells, mitochondrial dysfunction, and chronic inflammation. In the kidney, a metabolically demanding organ, this imbalance contributes to the pathogenesis of chronic kidney disease (CKD) and acute kidney injury (AKI). Senescent cells secrete a senescence-associated secretory phenotype, which amplifies inflammation, fibrosis, and tissue remodeling. The bidirectional interplay between impaired autophagy and cellular senescence exacerbates renal tubular atrophy, glomerulosclerosis, and interstitial fibrosis, thereby promoting CKD progression and maladaptive repair following AKI. Emerging therapeutic strategies, including autophagy activators, senolytics, antioxidants, and stem cell based interventions, have shown promise in restoring cellular homeostasis and delaying renal aging. Nonetheless, challenges remain in achieving cell type specific modulation while avoiding the deleterious effects of excessive activation. This review highlights recent advances in understanding the mechanistic interplay between autophagy and senescence in renal physiology and disease, outlines their contributions to CKD and AKI, and explores evolving therapeutic strategies aimed at restoring autophagic flux and eliminating senescent cells. Targeting the autophagy senescence axis represents a compelling avenue for precision therapy in kidney disease and may redefine future approaches in nephrology.
    Keywords:  AKI; Autophagy; CKD; Cellular senescence
    DOI:  https://doi.org/10.1007/s11033-025-11180-0
  11. Biomedicines. 2025 Oct 13. pii: 2490. [Epub ahead of print]13(10):
      Cannabidiol (CBD) is a non-psychotropic compound found in plants of the Cannabis genus, extensively studied for its therapeutic potential. Research has shown that CBD possesses anti-inflammatory, antioxidant, and regenerative properties, and may contribute to the recovery of neural and bone tissues. In light of the aging population and the resulting rise in neurodegenerative and osteodegenerative conditions, exploring novel therapeutic strategies that promote cellular regeneration is increasingly important. This review aims to compile and critically analyze key studies published in recent decades regarding the effects of CBD on the regeneration of the central and peripheral nervous systems, as well as bone tissue. Findings from in vivo studies indicate that CBD can attenuate inflammatory responses, inhibit oxidative stress, and modulate cellular pathways involved in tissue repair, thereby supporting neuronal and bone regeneration. Moreover, evidence suggests that CBD may protect cells from structural damage, enhancing the functional recovery of affected tissues. Despite scientific advances highlighting cannabidiol as a promising agent for bone and nerve regeneration, its therapeutic application still faces significant limitations. The primary challenge lies in the lack of robust clinical trials in humans, as most existing evidence is derived from in vitro and in vivo studies, making it difficult to confirm its efficacy and safety in clinical contexts. Additionally, CBD's low bioavailability-due to first-pass hepatic metabolism-hinders dose standardization and reduces the predictability of therapeutic outcomes. Compounding these issues are regulatory constraints and the persistent social stigma surrounding cannabis-derived compounds, which further impede their integration and acceptance in regenerative medicine. Therefore, future research is essential to validate the therapeutic benefits of CBD and to establish its clinical applicability in treating neurological and bone disorders.
    Keywords:  aging; bone regeneration; cannabidiol; central nervous system; human endocannabinoid system; inflammation; nerve regeneration; peripheral nervous system
    DOI:  https://doi.org/10.3390/biomedicines13102490
  12. Antioxidants (Basel). 2025 Oct 13. pii: 1228. [Epub ahead of print]14(10):
      Osteoarthritis (OA) is one of the most common joint diseases worldwide, which is characterized by degenerative changes in articular cartilage and secondary osteophyte formation. Numerous factors influence OA, including aging, obesity, joint injury and chronic overloading. Among them, the senescence of chondrocytes is one of the key factors leading to OA. Chondrocyte senescence can trigger inflammatory responses, extracellular matrix (ECM) degradation, mitochondrial dysfunction and oxidative stress (OS), and autophagy. Sirtuin 6 (SIRT6), as a deacetylase related to aging, can regulate chondrocyte senescence and plays a certain part in OA. SIRT6 regulates the number and membrane integrity of mitochondria, alleviates excessive Reactive Oxygen Species (ROS) in mitochondria and reduces inflammation-mediated mitochondrial damage. In addition, SIRT6 can also regulate the activity of antioxidant enzymes, inhibit excessive ROS induced by inflammatory factors, and alleviate OS. However, as aging progresses, the activity of SIRT6 will decrease. Activating the activity of SIRT6 becomes a potential therapeutic target and has a certain alleviating effect on the development of OA. The supplementation of nicotinamide adenine dinucleotide (NAD+) precursors and SIRT6-specific activators can increase SIRT6, alleviate chondrocyte senescence, and reduce OA. This paper aims to focus on mitochondrial dysfunction and OS to explore SIRT6's effects on OA chondrocytes' senescence under aging and summarize the potential therapeutic targets for activating SIRT6 to provide assistance for the improvement of OA.
    Keywords:  Sirtuin 6; aging; mitochondrial dysfunction; osteoarthritis; oxidative stress
    DOI:  https://doi.org/10.3390/antiox14101228
  13. Stem Cell Rev Rep. 2025 Oct 31.
      The liver is a highly versatile and resilient organ that is crucial for metabolism, detoxification, digestion, and immune regulation. Its remarkable regenerative capacity is driven primarily by two key cellular processes: hepatocyte polyploidy and cellular senescence. This review explores the complex roles of polyploidy, in which hepatocytes possess multiple chromosome sets, and senescence, characterized by irreversible cell cycle arrest, in maintaining liver homeostasis and facilitating regeneration. Polyploid hepatocytes increase genetic and metabolic diversity, enabling the liver to withstand stress and recover from injury through mechanisms such as compensatory regeneration, depolyploidization, and the fusion of extrinsic stem cells. Concurrently, cellular senescence acts as a protective barrier against uncontrolled cell proliferation and genomic instability while also promoting tissue repair via the senescence-associated secretory phenotype (SASP). The interplay between polyploidy and senescence is regulated by critical molecular pathways, including the Hippo, PI3K/Akt, and p53 signaling pathways, which balance cell proliferation, differentiation, and apoptosis. Additionally, this review discusses the therapeutic potential of targeting these processes to increase liver regeneration, prevent fibrosis, and reduce the risk of hepatocellular carcinoma (HCC). Emerging strategies such as senolytic drugs, stem cell therapies, and cytokine modulation offer promising avenues for treating chronic liver diseases. However, challenges remain in fully understanding the functional distinctions between diploid and polyploid hepatocytes and managing the dual roles of senescence. Future research should focus on molecular insights and targeted interventions to optimize liver health and regenerative outcomes.
    Keywords:  Cellular polyploidy; Cellular senescence; Liver regeneration; Nuclear polyploidy; Regulatory
    DOI:  https://doi.org/10.1007/s12015-025-11001-8
  14. Front Neurosci. 2025 ;19 1633835
      The circadian system regulates core physiological processes, including muscle regeneration, protein synthesis, and cellular homeostasis. Disruptions in circadian rhythms contribute to impaired muscle function in older adults, with age-related declines in muscle mass and regenerative capacity serving as major contributors to sarcopenia. Emerging evidence indicates that exercise-a powerful modulator of muscle adaptation-can also influence circadian regulation, offering a potential avenue to enhance muscle repair in aging populations. This review examines how physical activity interacts with circadian mechanisms in aged skeletal muscle, emphasizing key molecular and cellular pathways involved in muscle regeneration. Central circadian regulators such as Clock, BMAL1, and PER1 are discussed in the context of muscle protein turnover, satellite cell activity, and mitochondrial function. Aligning exercise timing with circadian rhythms is proposed as a promising strategy to enhance muscle recovery and functional capacity in older individuals. Furthermore, the review highlights the therapeutic potential of chrono-exercise to delay the onset of sarcopenia and promote healthy aging. By integrating insights from chronobiology, geroscience, and exercise physiology, this analysis underscores the importance of chrono-exercise in supporting muscle health during aging.
    Keywords:  aging; circadian rhythm; exercise timing; sarcopenia; skeletal muscle regeneration
    DOI:  https://doi.org/10.3389/fnins.2025.1633835
  15. Front Med (Lausanne). 2025 ;12 1665708
      Sarcopenia is a major health issue among the global aging population, with a prevalence of 10 to 30% in those over 60 years old. As age advances, the gradual decline in muscle mass and function leads to reduced ability to perform daily activities and significantly increases the risks of falls, fractures, disability, and mortality. Recent studies have shown that skeletal muscle is not only a locomotive organ but also an important endocrine organ that affects systemic metabolism by secreting a series of bioactive molecules known as myokines. The secretion patterns of myokines undergo significant changes during aging and the progression of sarcopenia. Protective factors such as IL-15 and IGF-1 decrease, while pathological factors like myostatin and Activin A increase. This imbalance subsequently leads to the continued decline in muscle mass and function, reflected in multiple mechanisms including disruption of protein synthesis and degradation, mitochondrial dysfunction, and chronic inflammatory states. This article systematically reviews the role of myokines in sarcopenia, clarifies their molecular mechanisms, and explores clinical application prospects, aiming to provide a theoretical basis and new intervention targets for the prevention and treatment of sarcopenia. Future research should focus on the dynamic changes, interactions, and targeted intervention strategies of myokines to address the challenges of global aging and improve the quality of life for the elderly population.
    Keywords:  muscle aging; muscle metabolism; myokines; sarcopenia; therapeutic interventions
    DOI:  https://doi.org/10.3389/fmed.2025.1665708
  16. Mater Today Bio. 2025 Dec;35 102417
      The persistence of inflammation and mitochondrial dysfunction poses considerable challenges in the process of diabetic wound healing. Evidence from earlier research has revealed the significant activation of inflammation-related pathways in diabetic wound tissues. Thus, controlling inflammation may be the key to resolving non-healing diabetic wounds. Natural product-derived naringenin (Nar) and curcumin (Cur) can synergistically exert anti-inflammatory effects and accelerate mitochondrial repair. These compounds can promote the repair of damaged cells by improving mitochondrial function (restoring membrane potential, alleviating calcium overload, and inhibiting mitochondrial reactive oxygen species [ROS] production). Furthermore, they can activate the Nrf2/HO-1 pathway to enhance endogenous antioxidant defenses (SOD and CAT) and upregulate anti-inflammatory pathways, thus effectively suppressing NF-κB-mediated inflammatory cascades. In this study, we constructed a self-assembled herbal nanoparticle delivery system (NC NPs) composed of Nar and Cur. To enhance the applicability of this system for skin wounds, we prepared NC@Gel, a biocompatible thermo-sensitive hydrogel loaded with the NC NPs. In vivo experiments confirmed that NC@Gel not only provided synergistic anti-inflammatory and antioxidant effects but also regulated the phenotypic transition of macrophages, inhibits the secretion of pro-inflammatory factors, and ultimately promotes tissue regeneration in diabetic wounds. These findings shed light on the molecular mechanism through which NC@Gel exerts therapeutic effects via the Nrf2/NF-κB/mitochondrial functional axis. Overall, this study provides a novel nanomedicine-based strategy that could be translated for the clinical treatment of diabetic chronic wounds.
    Keywords:  Diabetic wound; Herbal self-assembled nanoparticles; Inflammation; Mitochondrial dysfunction; Oxidative stress
    DOI:  https://doi.org/10.1016/j.mtbio.2025.102417
  17. Biomolecules. 2025 Oct 14. pii: 1452. [Epub ahead of print]15(10):
      Cardiovascular aging is a multifactorial and systemic process that contributes significantly to the global burden of cardiovascular disease, particularly in older populations. This review explores the molecular and cellular mechanisms underlying cardiovascular remodeling in age-related conditions such as hypertension, atrial fibrillation, atherosclerosis, and heart failure. Central to this process are chronic low-grade inflammation (inflammaging), oxidative stress, cellular senescence, and maladaptive extracellular matrix remodeling. These hallmarks of aging interact to impair endothelial function, promote fibrosis, and compromise cardiac and vascular integrity. Key molecular pathways-including the renin-angiotensin-aldosterone system, NF-κB, NLRP3 inflammasome, IL-6, and TGF-β signaling-contribute to the transdifferentiation of vascular cells, immune dysregulation, and progressive tissue stiffening. We also highlight the role of the senescence-associated secretory phenotype and mitochondrial dysfunction in perpetuating inflammatory and fibrotic cascades. Emerging molecular therapies offer promising strategies to reverse or halt maladaptive remodeling. These include senescence-targeting agents (senolytics), Nrf2 activators, RNA-based drugs, and ECM-modulating compounds such as MMP inhibitors. Additionally, statins and anti-inflammatory biologics (e.g., IL-1β inhibitors) exhibit pleiotropic effects that extend beyond traditional risk factor control. Understanding the molecular basis of remodeling is essential for guiding future research and improving outcomes in older adults at risk of CVD.
    Keywords:  RNA-based therapies; atherosclerosis; cardiovascular aging; cellular senescence; extracellular matrix remodeling; heart failure; inflammaging; senolytics
    DOI:  https://doi.org/10.3390/biom15101452
  18. Front Pharmacol. 2025 ;16 1657436
       Introduction: Aging is a progressive and irreversible process linked to a variety of diseases. Examination of the processes targeted by pharmacological treatments could potentially both extend lifespan and alleviate age-associated diseases. 20(S)-protopanaxadiol (20(S)-PPD), a primary ginsenoside metabolite, has many beneficial properties, although it`s anti-aging effects are unknown.
    Methods: Lifespan and behavioral assays were used to determine the effects of 20(S)-PPD on life span and healthy lifespan. Stress resistance was systematically determined under heat, oxidative, and chemical stress conditions. The target of 20(S)-PPD was identified by molecular docking and surface plasmon resonance. Investigation in mutant worms identified the signaling pathway and transcription factor mediating 20(S)-PPD-induced longevity.
    Results: 20(S)-PPD could significantly extend Caenorhabditis elegans (C. elegans) lifespan without affecting food intake and reproductive output. It also improved healthspan in aging worms by ameliorating locomotor deficits and suppressing lipofuscin accumulation. Furthermore, 20(S)-PPD enhanced stress resistance and reduced age-associated reactive oxygen species (ROS) levels. Mechanistically, 20(S)-PPD bound dose-dependently to the insulin receptor (IR) with a KD value of 8.59 μM. The life-extending effects of 20(S)-PPD involved the DAF-2/insulin/IGF-1 signaling (IIS) pathway, rather than other conserved pathways. Treatment with 20(S)-PPD promoted DAF-16/FOXO activation and nuclear translocation, leading to upregulated transcription of several antioxidant and detoxification-related genes, including lys-7, mtl-1, hsp-12.6, dod-3, sod-3, hsp-16.2, gst-4 and sms-1. 20(S)-PPD also upregulated the protein levels of SOD-3 and GST-4, known promoters of longevity in C. elegans.
    Conclusion: These findings demonstrate that IR is a molecular target of 20(S)-PPD and reveal a mechanism by which 20(S)-PPD promotes longevity and stress resistance, suggesting the potential of 20(S)-PPD in slowing aging and the development of age-associated disorders.
    Keywords:  20(S)-protopanaxadiol; Caenorhabditis elegans; DAF-16/FOXO; insulin/IGF-1 signaling pathway; longevity
    DOI:  https://doi.org/10.3389/fphar.2025.1657436
  19. Int J Biol Macromol. 2025 Oct 23. pii: S0141-8130(25)09060-9. [Epub ahead of print] 148503
      Ovarian follicular development occurs under chronic hypoxia, imposing significant stress on granulosa cells (GCs) and leading to hypoxia-induced apoptosis, a key factor in follicular atresia and impaired fertility. However, the intrinsic mechanisms enabling GCs to resist hypoxic apoptosis remain unclear. Emerging evidence suggests lactate, beyond its traditional role as a glycolytic byproduct, functions as a critical mediator of cellular stress adaptation. Here, we investigated whether lactate confers protection to porcine granulosa cells (pGCs) by activating mitophagy under hypoxic conditions and elucidated the underlying molecular pathways. Using pGCs subjected to normoxia and hypoxia, combined with pharmacological inhibitors, RNA interference targeting LDHA, HIF-1α, and PINK1, mitochondrial membrane potential assays, apoptosis detection, Western blotting, and mitochondrial-lysosomal co-localization imaging, we demonstrated that lactate depletion exacerbates mitochondrial dysfunction and apoptosis under hypoxia. Conversely, exogenous lactate supplementation attenuated these effects by stabilizing HIF-1α and enhancing PINK1-Parkin-mediated mitophagy. Inhibition of mitophagy via 3-MA or PINK1 knockdown abolished lactate's protective effects, highlighting mitophagy as essential for lactate-mediated cell survival. Cross-species validation in murine granulosa cells (mGCs) in vitro and in vivo confirmed the conservation of lactate's protective mechanisms, where lactate depletion impaired mitochondrial function and increased follicular apoptosis, while lactate supplementation restored mitochondrial integrity and granulosa cell viability. Our findings reveal a novel lactate-HIF-1α-PINK1 signaling axis critical for pGCs resilience to hypoxic stress, offering new therapeutic targets for ovarian disorders such as polycystic ovary syndrome and ovarian aging.
    Keywords:  Apoptosis; HIF-1α; Lactate; Mitophagy; PINK1; Parkin; Porcine granulosa cell
    DOI:  https://doi.org/10.1016/j.ijbiomac.2025.148503
  20. J Invest Dermatol. 2025 Oct 27. pii: S0022-202X(25)03499-2. [Epub ahead of print]
      An adequate wound healing response requires the coordination of intercellular signals between multiple cell types. Following skin injury, endothelial cells and fibroblasts provisionally replace the site of injury with newly vascularized granulation tissue. Given the spatial and temporal overlap of these two cell types in the healing response, we hypothesize that endothelial cell-derived extracellular vesicles (ECEVs) could provide a communication pathway by which ECs influence fibroblast behavior. In this study we investigated the effects of ECEVs on fibroblast function both in vitro and in vivo through a murine skin wound healing model. Transcriptomic analysis showed that the uptake of ECEVs by fibroblasts altered functions and pathways relating to cell division, ECM organization, and fibrosis. This gene signature resulted from upregulation of the transcription factor ETV1, which enhanced fibroblast susceptibility to FGF2 found on ECEVs. This transcriptomic analysis was functionally corroborated through in vitro assays in which fibroblasts demonstrated enhanced proliferation, cell cycle progression, and altered ECM deposition following ECEV treatment. Administration of ECEVs to healing mouse wounds led to increased collagen density and fibroblast quantity in the wound bed of scar tissue. Our study highlights a previously undefined role for ECEVs in regulating fibroblast function during wound repair.
    Keywords:  angiogenesis; exosome; extracellular matrix; tissue regeneration; wound repair
    DOI:  https://doi.org/10.1016/j.jid.2025.10.584
  21. Development. 2025 Oct 15. pii: dev205103. [Epub ahead of print]152(20):
      Stem cell behavior is tightly regulated by signals from the surrounding immune environment. Immune cells play an indispensable role in the maintenance, activation and differentiation of tissue-resident stem cells (TSCs). These interactions are dynamic and adapt across the lifespan, profoundly influencing regenerative capacity under both physiological and pathological conditions. Notably, immune dysfunction originating from aging hematopoietic stem cells (HSCs) disrupts tissue regeneration across distant organs, including the brain, muscle and skin. In this Review, we synthesize current knowledge on the interplay between HSC aging and TSC function, emphasizing how age-related changes in HSC-derived immune outputs impair local tissue homeostasis. We explore potential mechanisms underlying HSC-TSC communication, including inflammaging, cytokine signaling and the secretion of bioactive factors. Finally, we discuss emerging strategies aimed at rejuvenating aged HSCs, restoring immune equilibrium and enhancing systemic tissue regeneration. By linking systemic immune remodeling to local niche dysfunction, this Review proposes a hierarchical model in which HSC aging acts as a central regulator of tissue regenerative decline.
    Keywords:  Bone marrow; Hematopoietic stem cell; Immunomodulation; Immunosenescence; Inflammation; Systemic aging
    DOI:  https://doi.org/10.1242/dev.205103
  22. Front Physiol. 2025 ;16 1633607
      Since being articulated by Claude Bernard, and ultimately named by Walter Cannon, the theory of Homeostasis has been a conceptual and practical bedrock of physiology and medicine. Homeostasis addresses the idea that internal stability is a requirement for survival and proper functioning of organisms. A great variety of transformative changes associated with development and reproduction are not addressed by homeostasis. Two familiar examples of non-homeostatic transformative processes are metamorphosis and childbirth. In a previous paper the name "kinorhesis" was proposed for a physiological principle encompassing the processes that account for episodes of transformative changes during reproduction, growth, and development. Like changes brought about by natural selection, kinorhetic transformations can have profound effects on the fitness of the organism in new or changing environments. But unlike evolutionary changes, kinorhesis takes place within the lifetime of the individual rather than across generations. Kinorhetic transformative changes exist alongside homeostasis such that the physiology of kinorhesis articulates with that of homeostasis. In most instances homeostasis and kinorhesis exist cooperatively, but sometimes they come into conflict. This paper will elaborate the new theoretical framework of kinorhesis using examples from across the biological Kingdoms, and describing the types of physiological mechanisms that distinguish homeostasis and kinorhesis. Physiological regulatory processes that are responsible for homeostasis and kinorhesis include compartmentation, negative feedback (normalizing reflexes), positive feedback (amplifying reflexes), and sequential controls. Homeostasis and Kinorhesis set boundaries on processes that provide stability and transformation to physiology, and they provide an heuristic framework for discovery and education. Kinorhesis employs the full scope of physiology from cellular level functions through organ systems, behaviors, and morphological changes. All aspects of homeostasis and kinorhesis are consistent with conventional theories and processes of Darwinian evolution.
    Keywords:  development; fruit ripening; metamorphosis; negative feedback; positive feedback; quorum sensing; reproduction
    DOI:  https://doi.org/10.3389/fphys.2025.1633607
  23. Pathogens. 2025 Oct 16. pii: 1045. [Epub ahead of print]14(10):
      We hypothesize that a unified mitochondrial perspective on aging, HIV, and long COVID reveals shared pathogenic mechanisms and specific therapeutic vulnerabilities that are overlooked when these conditions are treated independently. Mitochondrial dysfunction is increasingly recognized as a common factor driving aging, HIV, and long COVID. Shared mechanisms-including oxidative stress, impaired mitophagy and dynamics, mtDNA damage, and metabolic reprogramming-contribute to ongoing energy failure and chronic inflammation. Recent advancements highlight new therapeutic strategies such as mitochondrial transfer, transplantation, and genome-level correction of mtDNA variants, with early preclinical and clinical studies providing proof-of-concept. This review summarizes current evidence on mitochondrial changes across aging and post-viral syndromes, examines emerging organelle-based therapies, and discusses key challenges related to safety, durability, and translation.
    Keywords:  HIV; SARS-CoV-2; mitochondria
    DOI:  https://doi.org/10.3390/pathogens14101045
  24. J Cell Mol Med. 2025 Nov;29(21): e70928
      Activation of the endoplasmic reticulum (ER) stress is an adaptive response to disturbed ER homeostasis caused by the accumulation of misfolded or unfolded proteins, or an acute increase in the entry of newly synthesised or mutated proteins into the ER lumen. Overwhelmed or prolonged ER stress causes apoptotic cell death or a maladaptive state of the cell, resulting in various pathological diseases including cancer, inflammation and aging. With a screening of a chemical compound library, here we show that inhibition of histone deacetylases (HDACs) induces ER stress, along with increased retro-translocation of misfolded proteins from the ER lumen to the cytosol for proteasomal degradation. HDAC inhibitors (HDACi) activate the PERK-eIF2α subbranch of the unfolded protein response (UPR), whereas the IRE1α and ATF6 pathways are not affected. Inhibition of the PERK subbranch with specific siRNA or a small molecule inhibitor ameliorates HDACi-induced apoptotic cell death. In addition, a non-phosphorylatable mutant of eIF2α, a critical substrate that transduces the PERK-mediated ER stress response, abolishes apoptosis induced by HDACi, but not by the DNA damage reagent doxorubicin. HDACi reduce the sizes of tumours formed from wildtype but not eIF2αS51A-mutant cells in a xenograft model, further demonstrating the involvement of the PERK subbranch in HDACi-induced ER stress and cell death. Our study reveals novel effects of the well-studied family of HDAC inhibitors, which can be explored further in clinics to treat certain types of cancer manifested with abnormal ER stress conditions.
    Keywords:  ER stress; HDAC inhibitors; PERK pathway; apoptosis; quisinostat; unfolded protein response
    DOI:  https://doi.org/10.1111/jcmm.70928
  25. Sci Adv. 2025 Oct 31. 11(44): eadt3014
      The integrated stress response (ISR) is a eukaryotic stress-responsive signaling pathway that attenuates global protein synthesis while allowing selective translation of specific mRNAs, which together can reestablish homeostasis following acute stress. Diverse pathologic insults activate one or more of the four ISR kinases, which selectively phosphorylate eIF2α to mediate ISR functions. Recent results suggest that enhancing ISR kinase activity could ameliorate pathologies linked to numerous diseases, including many neurodegenerative disorders. However, few pharmacological strategies exist to selectively activate ISR kinases and downstream adaptive signaling. Here, we report that compound A8 can preferentially activate the ISR through the binding of the cytosolic pattern recognition receptor RIG-I, which subsequently activates the heme-regulated inhibitor (HRI) ISR kinase independent of an interferon response. The establishment of A8 and its active metabolite CC81 provides opportunities to probe the biological and therapeutic relationship between innate immune signaling and ISR activation in health and disease.
    DOI:  https://doi.org/10.1126/sciadv.adt3014