Aging Cell最新文献

{"title":"Sexually Dimorphic Response to Dietary Restriction-Induced Longevity and Muscle Preservation in Nothobranchius furzeri.","authors":"Sonia Sandhi, Hannah Somers, Matthew Cox, Celeste Nobrega, Ryan Seaman, Elizabeth Baker, Olivia Lentchner, Robyn Reeve, Romain Menard, James Godwin, Anastasia Paulmann, Aric Rogers, Dario Riccardo Valenzano, Joel H Graber, Hermann Haller, Romain Madelaine","doi":"10.1111/acel.70791","DOIUrl":"10.1111/acel.70791","url":null,"abstract":"<p><p>Age-related skeletal muscle decline (sarcopenia) contributes to frailty and mortality, yet how sex influences muscle aging and dietary interventions remains unclear. Using the short-lived vertebrate Nothobranchius furzeri, we investigated how sex and intermittent fasting (IF) interact to regulate lifespan and skeletal muscle aging. We establish an IF regimen that extends lifespan in both males and females, despite trade-offs including reduced growth and reproductive output. Importantly, IF improves swimming performance in aged animals of both sexes. Under normal feeding, muscle aging exhibits pronounced sexual dimorphism. Males show age-associated myofiber hyperplasia, whereas females preserve fiber number but undergo hypertrophic remodeling. IF partially attenuates both phenotypes, maintaining a youthful fiber size distribution in males and females. Single-nucleus RNA-sequencing reveals sex-specific remodeling of muscle-fiber composition with age: females shift toward oxidative slow-twitch fibers under normal feeding, a change attenuated by IF, while males maintain relatively stable fiber-type proportions across diets. Cell-cell communication analyses show a global age-associated decline in intercellular signaling, with IF restoring distinct pathways in a sex-specific manner, including IGF signaling in females and metabolic ANGPTL signaling in males. Bulk transcriptomic profiling indicates largely sexually dimorphic aging trajectories, whereas IF induces both shared and sex-specific responses. Notably, IF upregulates ribosome biogenesis and genes supporting myofibrillar organization and contraction in both sexes, likely contributing to preserved muscle function. Together, these findings demonstrate that IF promotes longevity and muscle health through conserved anabolic mechanisms alongside sex-specific cellular preservation and adaptation, underscoring the importance of sex as a biological variable in interventions for healthy aging.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 11","pages":""},"PeriodicalIF":7.1,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13740022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149339977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Constitutive Activation of Skeletal Muscle mTORC1 Drives Pro-Inflammatory Gene Expression in Skeletal Muscle of Aged Mice.","authors":"Erik D Marchant, Hanna Kalenta, Jacquelyn May, Zhao Lai, Adam B Salmon, Blake B Rasmussen","doi":"10.1111/acel.70805","DOIUrl":"10.1111/acel.70805","url":null,"abstract":"<p><p>mTORC1 activity is increased in muscle with aging and is implicated as a potential driver of age-related declines in muscle health. While pharmacological inhibition of mTORC1 improves lifespan and healthspan, it remains unclear whether chronic activation of mTORC1 is sufficient to accelerate aging in skeletal muscle. We aimed to address this question using an inducible model of muscle-specific knockout of Depdc5, which encodes the protein DEP domain containing 5 (DEPDC5), a negative regulator of mTORC1. In 27-month-old mice, Depdc5 knockout induced a robust upregulation of inflammatory and immune-related genes, accompanied by alterations in metabolic and angiogenic pathways. Additionally, Depdc5 knockout mice exhibited an increase in TNF-α protein expression. However, these transcriptional and protein changes were not associated with an altered macrophage phenotype or with changes in muscle capillary density. Dietary rapamycin partially reversed mTORC1 signaling and some of the transcriptional changes, including those related to angiogenesis, but did not suppress inflammation-related transcripts or protein expression. These findings demonstrate that constitutive activation of mTORC1 is sufficient to drive pro-inflammatory changes in aged skeletal muscle, adding to the inflammation that already occurs with aging.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 11","pages":""},"PeriodicalIF":7.1,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13741394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149339973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Vicious Cycle of Sleep Disruption and Inflammaging: Mechanisms, Consequences, and Therapeutic Opportunities.","authors":"Fu-Ying Zhao, Jia-Mei Wang, Shi-Yang Lu, Liang Hao, Hai-Yan Zhang, Hua-Qin Wang","doi":"10.1111/acel.70798","DOIUrl":"10.1111/acel.70798","url":null,"abstract":"<p><p>Aging is characterized by two interdependent hallmarks: a chronic low-grade inflammatory state known as inflammaging, and a progressive deterioration of sleep and circadian rhythms. Emerging evidence indicates that these are not merely parallel processes but are mechanistically intertwined in a self-perpetuating cycle. This review synthesizes current knowledge on how age-related sleep and circadian disturbances exacerbate inflammaging through distinct molecular and cellular pathways. We examine the nocturnal dysregulation of the immune system, focusing on innate immune hyperactivation (e.g., via NLRP3 inflammasome and TLR4 signaling), cellular senescence (SASP), adaptive immune decline (T-cell aging), and disruption of systemic pathways such as the gut-brain axis. Clinical and epidemiological data link sleep disorders, particularly obstructive sleep apnea, to elevated inflammatory markers, accelerated epigenetic aging, and cognitive decline. Conversely, inflammaging impairs circadian regulatory structures, further degrading sleep quality. Interventions targeting the sleep-immune axis, including melatonin, circadian reinforcement, senotherapeutics, and lifestyle modifications, hold promise for mitigating inflammaging. We conclude that sleep disruption is not a passive symptom but an active driver of immunological aging, and propose that targeting this axis represents a viable strategy for promoting healthy longevity.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 11","pages":""},"PeriodicalIF":7.1,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13736552/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149331767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNMT1 Regulates Testosterone Synthesis in Aged Rat Leydig Cells via FTO-Mediated HSP90AA1 m⁶A Levels.","authors":"Yaqi Li, Yulei Duan, Zihang Tian, Yibing Gao, Yufei Qiao, Shuang Zhao, Wenyan Li, Zheng Gao, Siyun Niu","doi":"10.1111/acel.70760","DOIUrl":"10.1111/acel.70760","url":null,"abstract":"<p><p>Testosterone levels decline progressively with age from the third decade of life, impairing spermatogenesis and contributing to age-related disorders, underscoring the importance of enhancing endogenous testosterone production. DNA methyltransferase 1 (DNMT1) promotes testosterone synthesis in Leydig cells (LCs), yet the underlying mechanism remains unclear. Here, we found that DNMT1 expression is downregulated in aging rat testes and senescent LCs in vitro, correlating with reduced testosterone levels. Gain- and loss-of-function experiments confirmed that DNMT1 positively regulates testosterone synthesis and alleviates LC senescence, and that DNMT1 overexpression reverses the senescent phenotype and restores testosterone production. Mechanistically, RNA-seq of DNMT1-knockdown LCs identified FTO as a downstream target; DNMT1 suppresses FTO expression by promoting Fto promoter methylation. catRAPID prediction and RIP-qPCR validated Hsp90aa1 mRNA as a direct FTO substrate; FTO regulates HSP90AA1 expression through m⁶A modification, with DNMT1 indirectly modulating HSP90AA1 via FTO. Using HSP90AA1 overexpression, pharmacological inhibition, and rescue experiments, we confirmed that the DNMT1-FTO axis inhibits LC apoptosis through HSP90AA1-mediated AKT activation, thereby promoting testosterone synthesis. Expression patterns of this axis in aging rat testes and senescent LCs further corroborated its involvement in age-related testosterone dysregulation. In vivo AAV-mediated testicular DNMT1 knockdown recapitulated these findings. Collectively, our study elucidates the physiological role of DNMT1 in age-related testosterone decline and delineates the mechanism by which DNMT1 governs LC senescence and steroidogenic function, providing a potential therapeutic target for reproductive system aging.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70760"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658364/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149163868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Senescent Fibroblasts Impair B Cell Proliferation via Cell-Cell Contact.","authors":"Kassandra Vezyrgianni, Elizabeth MacLeod, Abigail Nutley, Yuchen Zhu, Alice E Denton","doi":"10.1111/acel.70766","DOIUrl":"10.1111/acel.70766","url":null,"abstract":"<p><p>Ageing profoundly impairs vaccine efficacy, leaving older individuals highly susceptible to infectious diseases despite vaccination. Although B cells retain the intrinsic capacity to generate germinal centre (GC) responses in older people, age-associated defects in T cells, dendritic cells and follicular dendritic cells (FDCs) limit the development of high-affinity, class-switched antibody responses. Here, we hypothesised that senescent fibroblasts disrupt B cell activation and expansion, thus contributing to the diminution of the humoral response in ageing. To test this hypothesis, we established an in vitro system in which human tonsil-derived YK6 fibroblasts expressing CD40L are co-cultured with PBMC-derived B cells. B cell activation, proliferation, and phenotype in response to low- and high-stimulation conditions was determined in co-culture with control or bleomycin-treated YK6 fibroblasts. Control YK6 fibroblasts promoted B-cell activation and proliferation in both 2D and 3D cultures, whereas bleomycin-treated fibroblasts robustly inhibited B-cell proliferation without impairing early activation. Conditioned media from bleomycin-treated fibroblasts partially reduced B cell proliferation, although to a lesser extent than direct co-culture, suggesting cell-cell contact was key to inhibiting B cell proliferation. Bleomycin-treated YK6 fibroblasts upregulated genes associated with impaired lymphocyte responses, such as PDCD1LG2, which may impact B cell activation. Indeed, B cells co-cultured with bleomycin-treated fibroblasts failed to fully initiate glycolysis and were essentially unable to synthesise new protein. Together, these findings suggest that senescence-like changes in fibroblasts could restrict B-cell proliferative capacity, which may contribute to impaired B cell responses in ageing.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70766"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13673512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149190107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elamipretide Rejuvenates Oocyte Quality and Restores Female Fertility During Reproductive Aging.","authors":"Hao-Lin Zhang, Yue Wang, Caizhu Wang, Xin Guo, Huanhua Chen, Yu-Xuan Hou, Xuan Wu, Zi-Jian Wu, Wen-Lin Pan, Rui-Jie Ma, Ping-Shuang Lu, Jinhui Shu, Shao-Chen Sun","doi":"10.1111/acel.70749","DOIUrl":"10.1111/acel.70749","url":null,"abstract":"<p><p>Aging represents a major contributor to the deterioration of female fertility, with oocyte quality being the central determinant of ovarian aging, a key factor underlying infertility. Although several natural compounds with anti-aging activity have been documented, highly effective strategies to reverse ovarian aging remain elusive. Here, we report that the peptide elamipretide preserves ovarian function and sustains female fertility during maternal aging. We found that elamipretide administration increases litter size in aged mice and ameliorates oocyte quality decline. Metabolomic and transcriptomic profiling revealed substantial restoration of multiple biological processes in aged oocytes after elamipretide injection. Elamipretide improved both nuclear and cytoplasmic maturation of aged oocytes, accompanied by enhanced cytoskeletal dynamics, mitochondrial metabolism, and organelle reorganization. Mechanistically, elamipretide alleviated age-associated oocyte maturation defects through synergistic activation of the vitamin B6-VEGF axis. Furthermore, elamipretide significantly promoted maturation, fertilization, and cleavage of aged human oocytes. Elamipretide treatment also rescued the developmental competence of porcine oocytes under oxidative damage. Collectively, this study identifies a novel peptide therapeutic candidate for aging-related infertility, showing that elamipretide restores the quality of aged oocytes for fertility by coordinately boosting nuclear and cytoplasmic maturation via activation of the VEGF signaling pathway.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70749"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13633435/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149101550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IGF-1/SLC25A33 Maintains Blood-Labyrinth Barrier Integrity by Suppressing TGF-β/Smad2-Mediated Pericyte Activation in Age-Related Hearing Loss.","authors":"Rui Xu, Jia Tang, Huan Lin, Qi Li, Yajin Feng, Xiaorong Zhang, Xiaohong Hu, Jiacai Yang, Yuhong Li, Yang Bai","doi":"10.1111/acel.70712","DOIUrl":"10.1111/acel.70712","url":null,"abstract":"<p><p>Age-related hearing loss (ARHL) is a prevalent sensory disorder in the elderly, yet the molecular mechanisms underlying cochlear aging remain incompletely understood. While insulin-like growth factor 1 (IGF-1) has been implicated in ARHL, its role in the stria vascularis, particularly in pericyte-mediated blood-labyrinth barrier (BLB) regulation, is poorly defined. We performed transcriptomic analysis of FACS-purified pericytes from young and aged mouse stria vascularis. Functional studies were conducted using primary pericyte cultures, lentiviral gene modulation, and AAV-mediated in vivo delivery. Auditory function was assessed by auditory brainstem response (ABR) and distortion product otoacoustic emissions (DPOAE). Molecular changes were evaluated via qPCR, western blot, immunofluorescence, flow cytometry, and transmission electron microscopy (TEM). Transcriptomics revealed significant downregulation of Igf1 and Slc25a33 in aged pericytes, with enrichment of the TGF-β signaling pathway. IGF-1 deficiency suppressed SLC25A33 expression in vitro, leading to mitochondrial ROS (mtROS) accumulation, activation of TGF-β/Smad2 signaling, and pericyte phenotypic switching, characterized by increased α-SMA and decreased E-cadherin. In vivo, suppression of IGF-1 or SLC25A33 activated TGF-β/Smad2 signaling in the stria vascularis, disrupted BLB ultrastructure, and exacerbated hearing loss. Conversely, exogenous IGF-1 or SLC25A33 overexpression attenuated these effects and partially restored auditory function. Our findings identify a novel IGF-1/SLC25A33-TGF-β/Smad2 axis that regulates pericyte activation and BLB integrity in the aging cochlea. This pathway provides mechanistic insight into ARHL pathogenesis and highlights a potential therapeutic target for preserving hearing in older adults.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70712"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13621939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149072907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"β-Catenin-Deficient Intervertebral Disc Cells Reduce Chemotactic Transcription and Myeloid Cell Recruitment to Injured Discs of Mice.","authors":"Tori M Kroon, Jazz Munitz, Anna Ranzenigo, Martin Umali, William Wang, Jonathan J Huang, Abraham J P Teunissen, Nilsson Holguin","doi":"10.1111/acel.70740","DOIUrl":"10.1111/acel.70740","url":null,"abstract":"<p><p>Aging exacerbates the incidence of discogenic chronic low back pain by excessive inflammation and immune cell presence. Aging reduces intervertebral disc (IVD) Wnt signaling, which is associated with IVD cell differentiation, IVD cell proliferation and anti-inflammatory signaling. However, it is unclear how in vivo Wnt signaling-absent IVD cells, which model aged IVD cells, regulate chemotactic signaling and immune cell recruitment. We hypothesized that Wnt signaling-absent IVD cells attenuate chemotactic transcription and immune cell recruitment to naive IVD and in response to IVD injury. First, because aging reduces Wnt signaling in all IVD cells, we deleted β-catenin using the AcanCreERT2. β-catenin deletion reduced monocyte chemoattractant protein-1 (MCP1/CCL2) Ccl2 in male and female IVDs by 58% and 79%, respectively (n = 5-6/sex). Using positron emission tomography/computed tomography (PET/CT) imaging of myeloid cells in 5-month-old mice (n = 4 IVD/sex/grp), deletion of β-catenin reduced myeloid-derived cell burden in naive IVD by 79% and attenuated IVD injury-induced recruitment by 48%. Next, because nucleus pulposus (NP) cells begin losing Wnt signaling early in life, we deleted β-catenin using the ShhCreERT2. Compared to RNA-sequencing of WT IVD post injury (n = 3/grp), deletion of β-catenin in NP cells impaired the activation of immune cell pathways, such as MCP1/CCL2. Together, the chemotactic transcriptomic response and myeloid cell accumulation due to IVD injury were impaired by the absence of IVD Wnt signaling transcription cofactor β-catenin. These data suggest that low-grade IVD inflammation and chronic IVD immune cell accumulation in aged IVD cells are regulated by IVD Wnt signaling.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70740"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13631559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149101697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protracted Fate Acquisition and Epigenetic De-Aging During Induced Neural Stem Cell Conversion of Human Blood Cells.","authors":"Lea Jessica Berg, Julia Franzen, Andreas Buness, Rachel Konang, Chao Sheng, Michael Peitz, Andreas Till, Wolfgang Wagner, Oliver Brüstle","doi":"10.1111/acel.70751","DOIUrl":"https://doi.org/10.1111/acel.70751","url":null,"abstract":"<p><p>Transcription factor-based direct conversion of somatic cells represents an interesting avenue for generating induced neural stem cells (iNSCs) from peripheral blood without transit through a pluripotent stage. While this paradigm has been shown to be associated with epigenetic de-aging, the dynamics of this process have remained unclear. Here, we used overexpression of the two reprogramming factors SOX2 and cMYC to generate iNSCs from erythroid progenitors of donors ranging from neonatal to 101 years of age. Using an epigenetic aging clock algorithm, we corroborated our previous finding that iNSCs generated from aged donors show pronounced epigenetic de-aging, preserving around 13% and 5% of the original donor age at low and high passages, respectively. Studying the dynamics of epigenetic de-aging during iNSC conversion across time, we found that this process is largely protracted, continuing for several weeks and even under proliferation-inhibiting conditions. Transcriptomic differences between young and old donor-derived iNSCs dissipate with extended time in conversion, too. Concordant with this observation, established iNSC lines lack age-associated cellular hallmarks, similar to induced pluripotent stem cells and their derivatives. Interestingly, time course analysis of DNA methylation and RNA sequencing data revealed that acquisition of a bona fide NSC signature extends greatly beyond the time point when proliferative PAX6-positive iNSCs emerge. The unexpected slow dynamics of these processes make iNSC conversion an attractive model for dissecting the mechanisms underlying somatic transdifferentiation and epigenetic de-aging.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70751"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13634082/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149101636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to \"A Non-Canonical Role for Hepatocyte MLKL in Promoting Mitochondrial Dysfunction and Senescence in the Aging Liver\".","authors":"","doi":"10.1111/acel.70746","DOIUrl":"10.1111/acel.70746","url":null,"abstract":"","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":"25 10","pages":"e70746"},"PeriodicalIF":7.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13633082/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149101567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}