Aging Cell最新文献

{"title":"A 209-Site DNA Methylation Predictor of Chronological Age Evaluated Under Empirical and Random Missingness.","authors":"Xiangteng Zhao, Yanhong Lu, Biqing Huang, Zijie Wang, Tong Yu, Ruoqi Zhao, Shiwen Yu, Shushan Wei, Yeting Zeng","doi":"10.1111/acel.70800","DOIUrl":"https://doi.org/10.1111/acel.70800","url":null,"abstract":"<p><p>DNA methylation age prediction from incomplete profiles requires evaluation under empirical and random missingness. We evaluated whole-blood chronological-age prediction using 524 development and 132 held-out GSE40279 samples and an external GSE73103 cohort (n = 355). Feature-stability analysis across 750 prespecified perturbation conditions identified a 209-CpG primary panel and a 52-CpG stringent sensitivity subset. The primary predictor combined five-nearest-neighbor reconstruction (KNN5) with Ridge regression. In the internal holdout, intact-profile prediction achieved a mean absolute error of 4.24 years, a root-mean-square error (RMSE) of 5.38 years, and Pearson r = 0.934. Under masks derived from 42 empirical templates of formalin-fixed paraffin-embedded detection failure, KNN5 reduced RMSE by 0.365 years relative to development-set mean replacement (95% bootstrap interval for the difference, -0.546 to -0.205), with larger reductions at higher missingness burdens. The reconstruction advantage persisted in complementary development analyses after randomization preserving both sample-level and CpG-level failure counts. External predictions remained associated with chronological age (r = 0.835), despite age-dependent calibration bias. Mixture analyses showed that background accuracy was central to target recovery as mixture asymmetry increased. These findings support local reconstruction within a stability-selected CpG panel for chronological-age prediction under the evaluated empirical and random missingness conditions.</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/PMC13724237/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149316277","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 Dietary Polyphenol Epigallocatechin Gallate Delays Biological Aging by Activating Peroxisome Biogenesis and Peroxisomal Fatty Acid β-Oxidation.","authors":"Xiaoming Huang, Yanfang Yang, Feng Huang, Wenwen Lin, Qiaowei Li, Yin Yuan, Pengli Zhu","doi":"10.1111/acel.70795","DOIUrl":"10.1111/acel.70795","url":null,"abstract":"<p><p>Epigallocatechin gallate (EGCG), a major tea polyphenol, has been proposed to promote healthy aging, but population-level evidence and underlying mechanisms remain unclear. We analyzed 10,977 participants from the National Health and Nutrition Examination Survey (NHANES) and conducted mechanistic studies in Caenorhabditis elegans and AML12 hepatocytes. Compared with non-consumers, both lower and higher EGCG intake categories were associated with lower PhenoAge acceleration, lower all-cause mortality, and higher estimated residual life expectancy. In C. elegans, EGCG supplementation extended lifespan and health span. Transcriptomics revealed upregulation of peroxisome-related genes. EGCG enhanced peroxisome biogenesis, as shown by increased peroxisome abundance, elevated prx-5 and prx-19 mRNA levels, and increases in PRX-5 and PRX-19 proteins. This increase in peroxisome capacity was accompanied by enhanced peroxisomal fatty acid β-oxidation, with increased mRNA levels of acox-1.2, acox-3, and dhs-28, increased ACOX-3 protein, and reduced very long-chain fatty acids (VLCFAs). Lipidomics showed enhanced processing of VLCFAs and accumulation of shorter-chain intermediates. Knockdown of prx-5, acox-1.2, or dhs-28 abolished EGCG-induced lifespan and health span benefits. In doxorubicin-induced senescent AML12 hepatocytes, EGCG reduced the proportion of SA-β-gal-positive cells and decreased p21 and p16 protein levels, while increasing peroxisome abundance and peroxisome-related proteins, including the biogenesis factors PEX5 and PEX19, the membrane transporters ABCD1 and PMP70, and the β-oxidation enzymes ACOX1, HSD17B4, EHHADH, and ACAA1. Conversely, the anti-senescent effects of EGCG were attenuated by Pex5 or Acox1 knockdown. Collectively, dietary EGCG intake is associated with slower biological aging, while experimental findings support peroxisome biogenesis and peroxisomal fatty acid β-oxidation in EGCG-mediated anti-aging effects.</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/PMC13727896/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149316352","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":"Role of Sirtuins in the Hallmarks of Skin Aging.","authors":"Rishabh Kala, Antonella Rella, Whitby Eagle, Earl Goyarts, Jian Cao, Binwei Deng, Kelly Dong, Chloe Schmit, Matthew Cappock, Krystle Corallo, Jacqueline Trivero","doi":"10.1111/acel.70789","DOIUrl":"10.1111/acel.70789","url":null,"abstract":"<p><p>Sirtuins are a family of enzymes that regulate cell homeostasis through pathways impacting genomic stability, mitochondrial function, cellular senescence, inflammation, and autophagy. In the skin, these pathways protect against extrinsic insults, maintain keratinocyte stem cells, and contribute to the overall structure and integrity of the skin barrier. Sirtuins decline with chronologic age, with UV exposure also impacting their activity, resulting in a loss of this homeostasis. There are 13 established biological hallmarks of aging. This review presents the current evidence of the mechanistic roles of sirtuins for each of these hallmarks, particularly in relation to skin.</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/PMC13740005/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149339976","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":"Exploring the Role of Transposable Elements to Sex Gap in Longevity in Three Drosophila Species.","authors":"Miriam Merenciano, Sonia Janillon, Camille Mermet-Bouvier, Nelly Burlet, Valentina Rodriguez-Rada, Victor Ronget, Patricia Gibert, Jean-Michel Gaillard, Jean-François Lemaitre, Gabriel A B Marais, Matthieu Boulesteix, Marie Fablet, Cristina Vieira","doi":"10.1111/acel.70788","DOIUrl":"10.1111/acel.70788","url":null,"abstract":"<p><p>In Drosophila, like other animal species, females tend to live longer than males, a phenomenon known as sex gap in longevity (SGL). One possible explanation could involve the activity of transposable elements (TE). TEs are normally repressed by epigenetic mechanisms, but this regulation weakens with age. Y chromosomes are enriched in TEs, and age-related TE activity may therefore be more pronounced in older males, likely affecting longevity (toxic Y hypothesis). Using three Drosophila species with different TE content, we showed that SGL varies among wild-type populations, reflecting both intra- and interspecies differences. Transcriptomic data revealed an age-related increase in TE-derived reads in D. melanogaster and D. suzukii, but not in D. simulans, with no differences between sexes. However, we observed a higher number of upregulated TE copies in older males compared to older females across the three species tested, which does not necessarily reflect increased transposition activity. Moreover, longevity assays did not reveal an association between increased TE expression and reduced lifespan. Finally, replacing the Y chromosome between strains with different SGL resulted in a progressive and strain-specific reduction of male lifespan in D. melanogaster, despite similar Y chromosome size. This was accompanied by gene expression changes and increased TE expression. In summary, our work calls for a reconsideration of the toxic Y hypothesis, suggesting it may be less relevant in species with low genomic TE content. Notably, Y chromosome effects on lifespan seem to be driven more by Y-linked heterochromatic polymorphisms and epistatic interactions than by overall TE abundance.</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/PMC13731165/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149316347","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":"Integrative Genetic and Single-Cell Analysis Reveals Macrophages as Key Mediators Linking Aging and Osteoporosis.","authors":"Xin Li, Meng-Yuan Yang, Si-Rui Gai, Peng Wei, Zeng-Hui Gu, Ming-Yu Han, Yue-Zhou Wu, Jia-Sheng Yu, Wang-Jun Chen, Zheng-Rui Liao, Jia-Xuan Gu, Jia-Dong Zhong, Pian-Pian Zhao, Ke Zhu, Ching-Lung Cheung, David Karasik, Hou-Feng Zheng","doi":"10.1111/acel.70812","DOIUrl":"10.1111/acel.70812","url":null,"abstract":"<p><p>Osteoporosis is a highly prevalent age-related disorder, and accumulating evidence suggests that it does not arise in isolation but is intrinsically linked to the aging process. Here, we employed integrative methods to systematically identify the relationship between aging and osteoporosis, and uncover the critical cell types and molecular regulators that mediate this association. Observational analysis of phenotypic data from UK Biobank and Mendelian Randomization analysis of summary-level statistics revealed that aging and osteoporosis are interrelated, acting as both causes and effects of each other. We identified macrophages as the key cell types mediating this association by integration of GWAS data with a comprehensively assembled single-cell transcriptomic atlas of bone remodeling. And the percentage of macrophages from bone marrow decreases with age. Additionally, shared genetic tools and weighted gene co-expression network analysis were employed to uncover novel molecular regulators underlying this crosstalk. We identified TGFB1 and a novel gene, HNRNPUL1, as key regulators that influence macrophages' differentiation and function. In conclusion, our study provides observational and genetic evidence for a bidirectional relationship between aging and osteoporosis and unveils a macrophage-centric mechanism regulated by TGFB1 and HNRNPUL1, offering new insights for age-related bone loss.</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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149356979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-Omics Reveals STAT1 as a Central Regulator of Oxidative Stress-Induced Senescence in the Aging Retina.","authors":"Yiran Fan, Ying Li, Xueying Wu, Lin Cai, Ruotong Yang, Zhenhui Liu, Yan Li, Bingtao Hao, Bo Lei, Xiuxiu Jin","doi":"10.1111/acel.70792","DOIUrl":"https://doi.org/10.1111/acel.70792","url":null,"abstract":"<p><p>Aging is the dominant risk factor for retinal neurodegeneration, yet the upstream regulators that coordinate senescence-associated programs across retinal cell types remain incompletely defined. Here we combined bulk RNA-seq and quantitative proteomics of retinas from naturally aged (24-month) and young (4-month) mice to define age-associated molecular programs and infer upstream regulators. We identified coordinated but imperfect transcript-protein coupling, with prominent immune and metabolic activation and concomitant repression of visual and structural pathways. Network-based integration nominated Stat1 as a convergent hub linking oxidative stress, inflammatory signaling, and cell fate regulation. Functionally, STAT1 induction accompanied oxidative stress-driven senescence in human ARPE-19 cells; ectopic STAT1 expression was sufficient to elicit senescence-like transcriptional changes, increase reactive oxygen species, and activate inflammasome-associated signaling, whereas STAT1 knockdown attenuated TBHP-induced senescence, reduced p53 and ASC upregulation, and blocked stress-induced nuclear accumulation of STAT1. Re-analysis of aging retina single-cell RNA-seq data further localized Stat1 expression primarily to horizontal cells and glial populations, while Stat1 target programs were engaged across multiple retinal cell types, consistent with compartmentalized initiation and multicellular propagation of inflammatory aging cues. Together, these data establish STAT1 as a mechanistic driver and cell-context-dependent marker of retinal aging, providing a rationale for targeting STAT1-centered pathways to delay or mitigate age-related retinal degeneration.</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":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149369720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MKP-2 Genetic Depletion Modulates Adipose Lipid Composition, Cellular Senescence, and Aging in Mice.","authors":"Morgan Welch, Nabin Ghimire, Shauri Smith, Cassandra Secunda, Alexis Fink, Alissar Sleiman, Laura Chambliss, Christopher Pinckard, Chloe Reyes, Priya Katta, Anna Ai, Benjamin R Harrison, Ahmed Lawan","doi":"10.1111/acel.70794","DOIUrl":"10.1111/acel.70794","url":null,"abstract":"<p><p>Aging is characterized by a gradual decline in physiological functions, impaired cellular repair mechanisms, and increased disease susceptibility. Mitogen-activated protein kinase phosphatase-2 (MKP-2) regulates diverse biological functions, including regulation of infection, brain activity, nutrient metabolism, and cell-cycle progression, but its role in senescence and adipose lipid metabolism in vivo remains unclear. Here, we investigated the effects of MKP-2 deficiency on cellular senescence and adipose lipid composition in aged mice using targeted lipidomics. MKP-2-deficient mouse embryonic fibroblasts (MEFs) and epididymal white adipose tissue (EWAT) exhibited reduced premature senescence. Lipidomic analysis revealed increased hexosylceramides (HexCERs) and phosphatidylglycerols (PG), and decreased diacylglycerols (DGs) in adipose tissue. These lipid alterations were accompanied by preserved lamin B1, reduced p53 phosphorylation, p16, and PAI-1, and increased JNK and Akt phosphorylation in EWAT. MKP-2 deficiency was also associated with extended lifespan and enhanced insulin responsiveness. Together, these studies identify MKP-2 as a potential regulator linking adipose lipid metabolism, stress-responsive signaling, cellular senescence, and aging, with its loss promoting a metabolically resilient adipose state that may contribute to improved systemic health and lifespan.</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/PMC13732110/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149316349","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":"Multidimensional MRI Reveals Cellular-Scale Microstructural Phenotypes in Human Brain Aging.","authors":"Joon Sik Park, Eppu Manninen, Shunxing Bao, Bennett A Landman, Yihong Yang, Dan Benjamini","doi":"10.1111/acel.70782","DOIUrl":"10.1111/acel.70782","url":null,"abstract":"<p><p>Brain aging is accompanied by profound cellular and microstructural changes that precede overt tissue loss, yet in vivo MRI studies largely emphasize macroscopic measures or isolated diffusion and relaxation metrics, providing limited insight into how cellular-scale tissue architecture is altered across the adult lifespan. Here, we apply multidimensional diffusion-relaxation MRI (MD-MRI) to map voxel-wise microstructural phenotypes in cognitively unimpaired adults spanning early adulthood to late life (23-77 years). Rather than relying on predefined compartment models, MD-MRI resolves continuous voxel-wise distributions in a joint diffusion-relaxation space, enabling an integrated, model-free description of how cellular shape, size, restriction, and chemical environment vary with age. Using this approach, we reveal age-related multilateral shifts within a complex microstructural landscape, marked by increasing heterogeneity and disorder across brain tissue. With age, cellular-scale features showed a systematic transition from small to larger length-scale structures accompanied by reduced microscopic restriction, indicating a loss of fine cellular barriers and expansion of extracellular space. In parallel, we show tissue-dependent alterations in fast-relaxing properties aligned with known gray- and white-matter aging processes, including iron accumulation and myelin loss. Together, these findings indicate that normative brain aging involves progressive reorganization of structure and composition at the cellular level, rather than uniform shifts in bulk tissue properties. By decoupling cellular-scale shape, size, restriction, and chemical environment in vivo, MD-MRI identifies increasing cellular heterogeneity and breakdown of microscopic restriction as central features of human brain aging and provides a biologically interpretable framework for linking microstructural reorganization to age-related functional decline.</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/PMC13731170/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149316350","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":"Mutation Accumulation Underpins Evolution of Lifespan Extension by Dietary Restriction.","authors":"Sara D Irish, Annabel Kimberley, Simone Immler, Jacob Moorad, Alexei A Maklakov","doi":"10.1111/acel.70808","DOIUrl":"10.1111/acel.70808","url":null,"abstract":"<p><p>Dietary restriction (DR) extends lifespan in animals and plants, but its evolutionary causes are elusive. The prevailing explanation is that DR prolongs life by shifting resources from reproduction to somatic maintenance. To test this idea in Caenorhabditis elegans we developed an experimental paradigm that tricks nematodes into increasing their reproductive effort under DR via food odour cues. Although DR improved survival, experimentally increased reproduction under DR did not reduce either immediate or long-term survival benefits, thus contradicting resource allocation theory. Our results suggest that much of the fertility suppression under DR reflects restraint from reproducing in a poor environment. We developed a model based on Hamilton's forces of selection showing that lifespan extension under DR can evolve because DR suppresses fertility, thereby directly increasing selection against mortality in that environment. Our novel analytical approach demonstrates that DR-driven lifespan extension can evolve under a broader range of conditions than previously anticipated, such as a relaxed need for physiological or genetic trade-offs. Instead, we show how reduced survival on plentiful food can evolve via mutation accumulation.</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/PMC13740021/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149339974","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":"Pyroptotic Macrophage Extracellular Vesicles Drive miR-103a-3p Mediated Mitochondrial Dysfunction in Granulosa Cells in Diminished Ovarian Reserve.","authors":"Wenhan Ju, Xin Xin, Yanli Xiao, Liwen Song, Jinfu Zhang, Shan Xiang","doi":"10.1111/acel.70806","DOIUrl":"10.1111/acel.70806","url":null,"abstract":"<p><p>To define the role of pyroptotic macrophage-derived extracellular vesicles (EVs) in diminished ovarian reserve (DOR) and to elucidate whether EVs-mediated transfer of miR-103a-3p drives mitochondrial dysfunction in granulosa cells. Single-cell RNA sequencing data from public GEO datasets were analyzed to characterize pyroptosis-associated features in ovarian macrophages across age groups. EVs were isolated from pyroptotic macrophages and applied to granulosa cells (KGN) to assess mitochondrial function, oxidative stress, and apoptosis. miRNA sequencing was performed to identify EVs-enriched miRNAs. miR-103a-3p expression was further evaluated in follicular fluid EVs from DOR patients and correlated with ovarian reserve markers. Mechanistic studies were conducted using in vitro assays and an in vivo mouse model. Pyroptosis signatures were enriched in ovarian macrophages with aging. EVs from pyroptotic macrophages were enriched in miR-103a-3p and induced mitochondrial dysfunction in granulosa cells, characterized by reduced ATP, increased ROS, and enhanced apoptosis; these effects were alleviated by miR-103a-3p inhibition. Clinically, miR-103a-3p was elevated in follicular fluid EVs from DOR patients and negatively correlated with AMH and AFC. Mechanistically, miR-103a-3p targeted MFN2 and BCL2L13, disrupting mitochondrial homeostasis in KGN cells. Restoration of these targets mitigated dysfunction in KGN cells. In vivo, AAV-mediated inhibition of miR-103a-3p improved follicular development and ovarian function. Pyroptotic macrophages may contribute to DOR progression through EVs-mediated delivery of miR-103a-3p, which impairs mitochondrial homeostasis in granulosa cells by targeting MFN2 and BCL2L13.</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/PMC13740007/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149339975","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}