Nature agingPub Date : 2025-02-05DOI: 10.1038/s43587-024-00797-8
Xinrong Zuo, Rui Zhao, Minming Wu, Yanyan Wang, Shisheng Wang, Kuo Tang, Yang Wang, Jie Chen, Xiaoxiang Yan, Yang Cao, Tao Li
{"title":"Multi-omic profiling of sarcopenia identifies disrupted branched-chain amino acid catabolism as a causal mechanism and therapeutic target","authors":"Xinrong Zuo, Rui Zhao, Minming Wu, Yanyan Wang, Shisheng Wang, Kuo Tang, Yang Wang, Jie Chen, Xiaoxiang Yan, Yang Cao, Tao Li","doi":"10.1038/s43587-024-00797-8","DOIUrl":"10.1038/s43587-024-00797-8","url":null,"abstract":"Sarcopenia is a geriatric disorder characterized by a gradual loss of muscle mass and function. Despite its prevalence, the underlying mechanisms remain unclear, and there are currently no approved treatments. In this study, we conducted a comprehensive analysis of the molecular and metabolic signatures of skeletal muscle in patients with impaired muscle strength and sarcopenia using multi-omics approaches. Across discovery and replication cohorts, we found that disrupted branched-chain amino acid (BCAA) catabolism is a prominent pathway in sarcopenia, which leads to BCAA accumulation and decreased muscle health. Machine learning analysis further supported the causal role of BCAA catabolic dysfunction in sarcopenia. Using mouse models, we validated that defective BCAA catabolism impairs muscle mass and strength through dysregulated mTOR signaling, and enhancing BCAA catabolism by BT2 protects against sarcopenia in aged mice and in mice lacking Ppm1k, a positive regulator of BCAA catabolism in skeletal muscle. This study highlights improving BCAA catabolism as a potential treatment of sarcopenia. Using multi-omics analysis, Zuo, Zhao, Wu, Wang, Wang and colleagues report disrupted branched-chain amino acid (BCAA) catabolism in skeletal muscle samples from patients with sarcopenia. In mouse models, they causally link BCAA catabolic dysfunction to impaired muscle mass and demonstrate the translational potential of enhancing BCAA catabolism.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 3","pages":"419-436"},"PeriodicalIF":17.0,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143257538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nature agingPub Date : 2025-02-05DOI: 10.1038/s43587-024-00799-6
Rabia R Khawaja, Adrián Martín-Segura, Olaya Santiago-Fernández, Rebecca Sereda, Kristen Lindenau, Mericka McCabe, Adrián Macho-González, Maryam Jafari, Aurora Scrivo, Raquel Gomez-Sintes, Bhakti Chavda, Ana Rosa Saez-Ibanez, Inmaculada Tasset, Esperanza Arias, Xianhong Xie, Mimi Kim, Susmita Kaushik, Ana Maria Cuervo
{"title":"Sex-specific and cell-type-specific changes in chaperone-mediated autophagy across tissues during aging.","authors":"Rabia R Khawaja, Adrián Martín-Segura, Olaya Santiago-Fernández, Rebecca Sereda, Kristen Lindenau, Mericka McCabe, Adrián Macho-González, Maryam Jafari, Aurora Scrivo, Raquel Gomez-Sintes, Bhakti Chavda, Ana Rosa Saez-Ibanez, Inmaculada Tasset, Esperanza Arias, Xianhong Xie, Mimi Kim, Susmita Kaushik, Ana Maria Cuervo","doi":"10.1038/s43587-024-00799-6","DOIUrl":"https://doi.org/10.1038/s43587-024-00799-6","url":null,"abstract":"<p><p>Aging leads to progressive decline in organ and tissue integrity and function, partly due to loss of proteostasis and autophagy malfunctioning. A decrease with age in chaperone-mediated autophagy (CMA), a selective type of lysosomal degradation, has been reported in various organs and cells from rodents and humans. Disruption of CMA recapitulates features of aging, whereas activating CMA in mice protects against age-related diseases such as Alzheimer's, retinal degeneration and/or atherosclerosis. However, sex-specific and cell-type-specific differences in CMA with aging remain unexplored. Here, using CMA reporter mice and single-cell transcriptomic data, we report that most organs and cell types show CMA decline with age, with males exhibiting a greater decline with aging. Reduced CMA is often associated with fewer lysosomes competent for CMA. Transcriptional downregulation of CMA genes may further contribute to CMA decline, especially in males. These findings suggest that CMA differences may influence organ vulnerability to age-related degeneration.</p>","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":17.0,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143257574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nature agingPub Date : 2025-02-03DOI: 10.1038/s43587-024-00793-y
Heike A. Bischoff-Ferrari, Stephanie Gängler, Maud Wieczorek, Daniel W. Belsky, Joanne Ryan, Reto W. Kressig, Hannes B. Stähelin, Robert Theiler, Bess Dawson-Hughes, René Rizzoli, Bruno Vellas, Laure Rouch, Sophie Guyonnet, Andreas Egli, E. John Orav, Walter Willett, Steve Horvath
{"title":"Individual and additive effects of vitamin D, omega-3 and exercise on DNA methylation clocks of biological aging in older adults from the DO-HEALTH trial","authors":"Heike A. Bischoff-Ferrari, Stephanie Gängler, Maud Wieczorek, Daniel W. Belsky, Joanne Ryan, Reto W. Kressig, Hannes B. Stähelin, Robert Theiler, Bess Dawson-Hughes, René Rizzoli, Bruno Vellas, Laure Rouch, Sophie Guyonnet, Andreas Egli, E. John Orav, Walter Willett, Steve Horvath","doi":"10.1038/s43587-024-00793-y","DOIUrl":"10.1038/s43587-024-00793-y","url":null,"abstract":"While observational studies and small pilot trials suggest that vitamin D, omega-3 and exercise may slow biological aging, larger clinical trials testing these treatments individually or in combination are lacking. Here, we report the results of a post hoc analysis among 777 participants of the DO-HEALTH trial on the effect of vitamin D (2,000 IU per day) and/or omega-3 (1 g per day) and/or a home exercise program on four next-generation DNA methylation (DNAm) measures of biological aging (PhenoAge, GrimAge, GrimAge2 and DunedinPACE) over 3 years. Omega-3 alone slowed the DNAm clocks PhenoAge, GrimAge2 and DunedinPACE, and all three treatments had additive benefits on PhenoAge. Overall, from baseline to year 3, standardized effects ranged from 0.16 to 0.32 units (2.9–3.8 months). In summary, our trial indicates a small protective effect of omega-3 treatment on slowing biological aging over 3 years across several clocks, with an additive protective effect of omega-3, vitamin D and exercise based on PhenoAge. Applying epigenetic clocks to samples from the DO-HEALTH trial, Bischoff-Ferrari et al. report a small protective effect of omega-3 supplementation over 3 years on several clocks and an additive protective effect of omega-3, vitamin D and exercise using PhenoAge.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 3","pages":"376-385"},"PeriodicalIF":17.0,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s43587-024-00793-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143124149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nature agingPub Date : 2025-01-31DOI: 10.1038/s43587-025-00811-7
Yang Yang, Natacha Jn-Simon, Yonghan He, Chunbao Sun, Peiyi Zhang, Wanyi Hu, Tian Tian, Huadong Zeng, Sreenivasulu Basha, Araceli S. Huerta, Lu-Zhe Sun, Xian-Ming Yin, Robert Hromas, Guangrong Zheng, Liya Pi, Daohong Zhou
{"title":"A BCL-xL/BCL-2 PROTAC effectively clears senescent cells in the liver and reduces MASH-driven hepatocellular carcinoma in mice","authors":"Yang Yang, Natacha Jn-Simon, Yonghan He, Chunbao Sun, Peiyi Zhang, Wanyi Hu, Tian Tian, Huadong Zeng, Sreenivasulu Basha, Araceli S. Huerta, Lu-Zhe Sun, Xian-Ming Yin, Robert Hromas, Guangrong Zheng, Liya Pi, Daohong Zhou","doi":"10.1038/s43587-025-00811-7","DOIUrl":"10.1038/s43587-025-00811-7","url":null,"abstract":"Accumulation of senescent cells (SnCs) plays a causative role in many age-related diseases and has also been implicated in the pathogenesis and progression of metabolic dysfunction-associated steatotic liver disease (MASLD). Senolytics that can selectively kill SnCs have the potential to be developed as therapeutics for these diseases. Here we report the finding that 753b, a dual BCL-xL/BCL-2 proteolysis-targeting chimera (PROTAC), acts as a potent and liver-tropic senolytic. We found that treatment with 753b selectively reduced SnCs in the liver in aged mice and STAM mice in part due to its sequestration in the liver. Moreover, 753b treatment could effectively reduce the progression of MASLD and the development of hepatocellular carcinoma (HCC) in STAM mice even after the mice developed substantial metabolic dysfunction-associated steatohepatitis (MASH) and hepatic fibrosis. These findings suggest that BCL-xL/BCL-2 PROTACs have the potential to be developed as therapeutics for MASLD to reduce MASH-driven HCC. Yang, Jn-Simon, He et al. report that the dual BCL-xL/BCL-2 PROTAC 753b is a potent and liver-tropic senolytic, which (unlike other inhibitors of BCL-xL) does not cause severe thrombocytopenia. They evaluate its efficacy in natural aging and in reducing progression from steatotic liver disease to hepatocellular carcinoma, using mouse models.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 3","pages":"386-400"},"PeriodicalIF":17.0,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nature agingPub Date : 2025-01-31DOI: 10.1038/s43587-024-00802-0
Chien-Wei Lee, Belle Yu-Hsuan Wang, Shing Hei Wong, Yi-Fan Chen, Qin Cao, Allen Wei-Ting Hsiao, Sin-Hang Fung, Yu-Fan Chen, Hao-Hsiang Wu, Po-Yu Cheng, Zong-Han Chou, Wayne Yuk-Wai Lee, Stephen Kwok Wing Tsui, Oscar Kuang-Sheng Lee
{"title":"Ginkgolide B increases healthspan and lifespan of female mice","authors":"Chien-Wei Lee, Belle Yu-Hsuan Wang, Shing Hei Wong, Yi-Fan Chen, Qin Cao, Allen Wei-Ting Hsiao, Sin-Hang Fung, Yu-Fan Chen, Hao-Hsiang Wu, Po-Yu Cheng, Zong-Han Chou, Wayne Yuk-Wai Lee, Stephen Kwok Wing Tsui, Oscar Kuang-Sheng Lee","doi":"10.1038/s43587-024-00802-0","DOIUrl":"10.1038/s43587-024-00802-0","url":null,"abstract":"Various anti-aging interventions show promise in extending lifespan, but many are ineffective or even harmful to healthspan. Ginkgolide B (GB), derived from Ginkgo biloba, reduces aging-related morbidities such as osteoporosis, yet its effects on healthspan and longevity have not been fully understood. In this study, we found that continuous oral administration of GB to female mice beginning at 20 months of age extended median survival and median lifespan by 30% and 8.5%, respectively. GB treatment also decreased tumor incidence; enhanced muscle quality, physical performance and metabolism; and reduced systemic inflammation and senescence. Single-nucleus RNA sequencing of skeletal muscle tissue showed that GB ameliorated aging-associated changes in cell type composition, signaling pathways and intercellular communication. GB reduced aging-induced Runx1+ type 2B myonuclei through the upregulation of miR-27b-3p, which suppresses Runx1 expression. Using functional analyses, we found that Runx1 promoted senescence and cell death in muscle cells. Collectively, these findings suggest the translational potential of GB to extend healthspan and lifespan and to promote healthy aging. Lee et al. demonstrate that Ginkgolide B treatment extends lifespan and enhances healthspan in female mice, including a reduction in tumor incidence, enhancement in muscle quality and function and suppression of systemic inflammation and senescence.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 2","pages":"237-258"},"PeriodicalIF":17.0,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nature agingPub Date : 2025-01-29DOI: 10.1038/s43587-025-00804-6
Methodios Ximerakis, Kristina M. Holton, Richard M. Giadone, Ceren Ozek, Monika Saxena, Samara Santiago, Xian Adiconis, Danielle Dionne, Lan Nguyen, Kavya M. Shah, Jill M. Goldstein, Caterina Gasperini, Ioannis A. Gampierakis, Scott L. Lipnick, Sean K. Simmons, Sean M. Buchanan, Amy J. Wagers, Aviv Regev, Joshua Z. Levin, Lee L. Rubin
{"title":"Author Correction: Heterochronic parabiosis reprograms the mouse brain transcriptome by shifting aging signatures in multiple cell types","authors":"Methodios Ximerakis, Kristina M. Holton, Richard M. Giadone, Ceren Ozek, Monika Saxena, Samara Santiago, Xian Adiconis, Danielle Dionne, Lan Nguyen, Kavya M. Shah, Jill M. Goldstein, Caterina Gasperini, Ioannis A. Gampierakis, Scott L. Lipnick, Sean K. Simmons, Sean M. Buchanan, Amy J. Wagers, Aviv Regev, Joshua Z. Levin, Lee L. Rubin","doi":"10.1038/s43587-025-00804-6","DOIUrl":"10.1038/s43587-025-00804-6","url":null,"abstract":"","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 2","pages":"333-333"},"PeriodicalIF":17.0,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s43587-025-00804-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nature agingPub Date : 2025-01-29DOI: 10.1038/s43587-024-00798-7
Dorsa Toghani, Sanika Gupte, Sharon Zeng, Elmir Mahammadov, Edie I Crosse, Negar Seyedhassantehrani, Christian Burns, David Gravano, Stefan Radtke, Hans-Peter Kiem, Sonia Rodriguez, Nadia Carlesso, Amogh Pradeep, Alexis Georgiades, Fabienne Lucas, Nicola K Wilson, Sarah J Kinston, Berthold Göttgens, Le Zong, Isabel Beerman, Bongsoo Park, Derek H Janssens, Daniel Jones, Ali Toghani, Claus Nerlov, Eric M Pietras, Marion Mesnieres, Christa Maes, Atsushi Kumanogoh, Thomas Worzfeld, Jin-Gyu Cheong, Steven Z Josefowicz, Peter Kharchenko, David T Scadden, Antonio Scialdone, Joel A Spencer, Lev Silberstein
{"title":"Niche-derived Semaphorin 4A safeguards functional identity of myeloid-biased hematopoietic stem cells.","authors":"Dorsa Toghani, Sanika Gupte, Sharon Zeng, Elmir Mahammadov, Edie I Crosse, Negar Seyedhassantehrani, Christian Burns, David Gravano, Stefan Radtke, Hans-Peter Kiem, Sonia Rodriguez, Nadia Carlesso, Amogh Pradeep, Alexis Georgiades, Fabienne Lucas, Nicola K Wilson, Sarah J Kinston, Berthold Göttgens, Le Zong, Isabel Beerman, Bongsoo Park, Derek H Janssens, Daniel Jones, Ali Toghani, Claus Nerlov, Eric M Pietras, Marion Mesnieres, Christa Maes, Atsushi Kumanogoh, Thomas Worzfeld, Jin-Gyu Cheong, Steven Z Josefowicz, Peter Kharchenko, David T Scadden, Antonio Scialdone, Joel A Spencer, Lev Silberstein","doi":"10.1038/s43587-024-00798-7","DOIUrl":"10.1038/s43587-024-00798-7","url":null,"abstract":"<p><p>Somatic stem cell pools comprise diverse, highly specialized subsets whose individual contribution is critical for the overall regenerative function. In the bone marrow, myeloid-biased hematopoietic stem cells (myHSCs) are indispensable for replenishment of myeloid cells and platelets during inflammatory response but, at the same time, become irreversibly damaged during inflammation and aging. Here we identify an extrinsic factor, Semaphorin 4A (Sema4A), which non-cell-autonomously confers myHSC resilience to inflammatory stress. We show that, in the absence of Sema4A, myHSC inflammatory hyper-responsiveness in young mice drives excessive myHSC expansion, myeloid bias and profound loss of regenerative function with age. Mechanistically, Sema4A is mainly produced by neutrophils, signals via a cell surface receptor, Plexin D1, and safeguards the myHSC epigenetic state. Our study shows that, by selectively protecting a distinct stem cell subset, an extrinsic factor preserves functional diversity of somatic stem cell pool throughout organismal lifespan.</p>","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":17.0,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nature agingPub Date : 2025-01-27DOI: 10.1038/s43587-025-00807-3
Bernadette Hotzi, Tibor Vellai
{"title":"Transposable element methylation tracks age","authors":"Bernadette Hotzi, Tibor Vellai","doi":"10.1038/s43587-025-00807-3","DOIUrl":"10.1038/s43587-025-00807-3","url":null,"abstract":"In mammals, the 5-methylcytosine epigenetic mark is mostly located in transposable elements, which are repetitive intragenomic parasites. In this issue of Nature Aging, Gorbunova and colleagues show that 5-methylcytosine levels in certain LINE1 retrotransposon loci highly correlate with age and the incidence of certain pathologies. Thus, LINE1 (the only known transposable element family capable of autonomous jumping in the human genome) serves as a suitable DNA template for accurately determining age and predicting disease.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 2","pages":"179-181"},"PeriodicalIF":17.0,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nature agingPub Date : 2025-01-16DOI: 10.1038/s43587-024-00773-2
Gabrielle Gilmer, Hirotaka Iijima, Zachary R. Hettinger, Natalie Jackson, Juliana Bergmann, Allison C. Bean, Nafiseh Shahshahan, Ekaterina Creed, Rylee Kopchak, Kai Wang, Hannah Houston, Jonathan M. Franks, Michael J. Calderon, Claudette St Croix, Rebecca C. Thurston, Christopher H. Evans, Fabrisia Ambrosio
{"title":"Menopause-induced 17β-estradiol and progesterone loss increases senescence markers, matrix disassembly and degeneration in mouse cartilage","authors":"Gabrielle Gilmer, Hirotaka Iijima, Zachary R. Hettinger, Natalie Jackson, Juliana Bergmann, Allison C. Bean, Nafiseh Shahshahan, Ekaterina Creed, Rylee Kopchak, Kai Wang, Hannah Houston, Jonathan M. Franks, Michael J. Calderon, Claudette St Croix, Rebecca C. Thurston, Christopher H. Evans, Fabrisia Ambrosio","doi":"10.1038/s43587-024-00773-2","DOIUrl":"10.1038/s43587-024-00773-2","url":null,"abstract":"Female individuals who are post-menopausal present with higher incidence of knee osteoarthritis (KOA) than male counterparts; however, the mechanisms underlying this disparity are unknown. The most commonly used preclinical models lack human-relevant menopausal phenotypes, which may contribute to our incomplete understanding of sex-specific differences in KOA pathogenesis. Here we chemically induced menopause in middle-aged (14–16 months) C57/BL6N female mice. When we mapped the trajectory of KOA over time, we found that menopause aggravated cartilage degeneration relative to non-menopause controls. Network medicine analyses revealed that loss of 17β-estradiol and progesterone with menopause enhanced susceptibility to senescence and extracellular matrix disassembly. In vivo, restoration of 17β-estradiol and progesterone in menopausal mice protected against cartilage degeneration compared to untreated menopausal controls. Accordingly, post-menopausal human chondrocytes displayed decreased markers of senescence and increased markers of chondrogenicity when cultured with 17β-estradiol and progesterone. These findings implicate menopause-associated senescence and extracellular matrix disassembly in the sex-specific pathogenesis of KOA. Knee osteoarthritis has a sex-specific phenotype with post-menopausal persons experiencing the highest incidence. Here the authors investigate the underlying mechanisms in a mouse model of menopause and find that the loss of 17β-estradiol and progesterone enhanced susceptibility to senescence, extracellular matrix disassembly and cartilage degradation.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 1","pages":"65-86"},"PeriodicalIF":17.0,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142995867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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