Pub Date : 2025-10-17DOI: 10.1038/s43587-025-00993-0
Vittorio Dibello, Frank Lobbezoo, Vincenzo Solfrizzi, Francesco Panza
Through biological, functional and psychosocial pathways that include inflammation, malnutrition and social isolation, oral health and disease contributes to systemic aging and frailty. Building on the concept of oral frailty, here we argue that validated oral health indicators — which are widely captured in aging surveys — should be integrated into multidimensional frailty frameworks to improve prediction, early intervention and holistic care for older adults.
{"title":"Embedding oral health indicators into multidimensional frailty models","authors":"Vittorio Dibello, Frank Lobbezoo, Vincenzo Solfrizzi, Francesco Panza","doi":"10.1038/s43587-025-00993-0","DOIUrl":"10.1038/s43587-025-00993-0","url":null,"abstract":"Through biological, functional and psychosocial pathways that include inflammation, malnutrition and social isolation, oral health and disease contributes to systemic aging and frailty. Building on the concept of oral frailty, here we argue that validated oral health indicators — which are widely captured in aging surveys — should be integrated into multidimensional frailty frameworks to improve prediction, early intervention and holistic care for older adults.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 12","pages":"2359-2362"},"PeriodicalIF":19.4,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145314446","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}
Pub Date : 2025-10-17DOI: 10.1038/s43587-025-00981-4
David Ezuz, Heba Ombashe, Lana Watad, Akmaral Rakhymzhanova, Satyarth Pandey, Orna Atar, Esther G. Meyron-Holtz, Noga Ron-Harel
Mechanisms of T cell aging involve cell-intrinsic alterations and interactions with immune and stromal cells. Here we found that splenic T cells exhibit greater functional decline than lymph node T cells within the same aged mouse, prompting investigation into how the aged spleen contributes to T cell aging. Proteomic analysis revealed increased expression of heme detoxification in aged spleen-derived lymphocytes. Exposure to the heme- and iron-rich aged splenic microenvironment induced aging phenotypes in young T cells, including reduced proliferation and CD39 upregulation. T cells survived this hostile niche by maintaining a low labile iron pool, at least in part, via IRP2 downregulation to resist ferroptosis but failed to induce sufficient iron uptake for activation. Iron supplementation enhanced antigen-specific T cell responses in aged mice. This study identifies the aged spleen as a source of hemolytic signals that systemically impair T cell function, underscoring a trade-off between T cell survival and function and implicating iron metabolism in immune aging. In their study, Ezuz et al. show that the aged spleen contributes to T cell aging through hemolytic stress and an increasingly heme- and iron-rich microenvironment. T cells adapt by limiting their iron levels. This protective response impairs cell function but can be reversed in vivo by iron supplementation during activation.
{"title":"Heme and iron toxicity in the aged spleen impairs T cell immunity through iron deprivation","authors":"David Ezuz, Heba Ombashe, Lana Watad, Akmaral Rakhymzhanova, Satyarth Pandey, Orna Atar, Esther G. Meyron-Holtz, Noga Ron-Harel","doi":"10.1038/s43587-025-00981-4","DOIUrl":"10.1038/s43587-025-00981-4","url":null,"abstract":"Mechanisms of T cell aging involve cell-intrinsic alterations and interactions with immune and stromal cells. Here we found that splenic T cells exhibit greater functional decline than lymph node T cells within the same aged mouse, prompting investigation into how the aged spleen contributes to T cell aging. Proteomic analysis revealed increased expression of heme detoxification in aged spleen-derived lymphocytes. Exposure to the heme- and iron-rich aged splenic microenvironment induced aging phenotypes in young T cells, including reduced proliferation and CD39 upregulation. T cells survived this hostile niche by maintaining a low labile iron pool, at least in part, via IRP2 downregulation to resist ferroptosis but failed to induce sufficient iron uptake for activation. Iron supplementation enhanced antigen-specific T cell responses in aged mice. This study identifies the aged spleen as a source of hemolytic signals that systemically impair T cell function, underscoring a trade-off between T cell survival and function and implicating iron metabolism in immune aging. In their study, Ezuz et al. show that the aged spleen contributes to T cell aging through hemolytic stress and an increasingly heme- and iron-rich microenvironment. T cells adapt by limiting their iron levels. This protective response impairs cell function but can be reversed in vivo by iron supplementation during activation.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 11","pages":"2247-2262"},"PeriodicalIF":19.4,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s43587-025-00981-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145314485","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}
Pub Date : 2025-10-16DOI: 10.1038/s43587-025-01008-8
A single blood-based test that measures several tau biomarkers enabled biological staging of Alzheimer’s disease. This approach not only indicated how advanced the disease was but also helped to predict its progression. This blood-based test could be highly valuable for patient management and for identifying individuals who are most likely to benefit from targeted therapies.
{"title":"A single blood test could reveal the biological stage of Alzheimer’s disease","authors":"","doi":"10.1038/s43587-025-01008-8","DOIUrl":"10.1038/s43587-025-01008-8","url":null,"abstract":"A single blood-based test that measures several tau biomarkers enabled biological staging of Alzheimer’s disease. This approach not only indicated how advanced the disease was but also helped to predict its progression. This blood-based test could be highly valuable for patient management and for identifying individuals who are most likely to benefit from targeted therapies.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 11","pages":"2160-2161"},"PeriodicalIF":19.4,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145310606","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}
Pub Date : 2025-10-14DOI: 10.1038/s43587-025-00971-6
Dahun Seo, Anh N. Do, Gyujin Heo, Jiseon Kwon, Soomin Song, Catherine Apio, Cheolmin Matthew Lee, Jigyasha Timsina, Katherine Gong, Yike Chen, Menghan Liu, Pat Kohlfeld, John Budde, Merce Boada, Adelina Orellana, Maria Victoria Fernandez, Agustin Ruiz, John C. Morris, Suzanne E. Schindler, Laura Ibanez, Taesung Park, Carlos Cruchaga, Yun Ju Sung
Age and APOE ε4 are major risk factors for Alzheimer’s disease (AD), while sex differences exist in disease prevalence and progression. Cerebrospinal fluid (CSF) proteomics can provide additional insights into brain aging and AD. To examine proteomic changes due to age, sex and apolipoprotein E (APOE) ε4 along with amyloid status before clinical AD occurs, we profiled 6,175 proteins in the CSF from 994 cognitively normal individuals aged 43–91 years. We identified and replicated 2,172 age-associated, 711 sex-associated, 193 APOE ε4-associated and 1,807 amyloid-associated proteins, with extensive overlap suggesting their interplay. These CSF-specific signatures were distinct from those in plasma. Network analysis revealed two proteomic modules—M2 (age-associated, sex-associated and amyloid-associated) and M6 (age-associated and sex-associated)—which were linked to neuropsychiatric and aging-related diseases. Together, our study provides proteomic changes during the early phase of AD, which may help identify new therapeutic targets of AD. Seo et al. present a cerebrospinal fluid (CSF) proteomic profiling of cognitively normal individuals, identifying age-associated, sex-associated, APOE ε4-associated and amyloid-associated changes. They unveil early Alzheimer’s disease CSF-specific proteomic signatures and potential therapeutic targets.
{"title":"Cerebrospinal fluid proteomic signatures in cognitively normal individuals identify distinct clusters linked to neurodegeneration","authors":"Dahun Seo, Anh N. Do, Gyujin Heo, Jiseon Kwon, Soomin Song, Catherine Apio, Cheolmin Matthew Lee, Jigyasha Timsina, Katherine Gong, Yike Chen, Menghan Liu, Pat Kohlfeld, John Budde, Merce Boada, Adelina Orellana, Maria Victoria Fernandez, Agustin Ruiz, John C. Morris, Suzanne E. Schindler, Laura Ibanez, Taesung Park, Carlos Cruchaga, Yun Ju Sung","doi":"10.1038/s43587-025-00971-6","DOIUrl":"10.1038/s43587-025-00971-6","url":null,"abstract":"Age and APOE ε4 are major risk factors for Alzheimer’s disease (AD), while sex differences exist in disease prevalence and progression. Cerebrospinal fluid (CSF) proteomics can provide additional insights into brain aging and AD. To examine proteomic changes due to age, sex and apolipoprotein E (APOE) ε4 along with amyloid status before clinical AD occurs, we profiled 6,175 proteins in the CSF from 994 cognitively normal individuals aged 43–91 years. We identified and replicated 2,172 age-associated, 711 sex-associated, 193 APOE ε4-associated and 1,807 amyloid-associated proteins, with extensive overlap suggesting their interplay. These CSF-specific signatures were distinct from those in plasma. Network analysis revealed two proteomic modules—M2 (age-associated, sex-associated and amyloid-associated) and M6 (age-associated and sex-associated)—which were linked to neuropsychiatric and aging-related diseases. Together, our study provides proteomic changes during the early phase of AD, which may help identify new therapeutic targets of AD. Seo et al. present a cerebrospinal fluid (CSF) proteomic profiling of cognitively normal individuals, identifying age-associated, sex-associated, APOE ε4-associated and amyloid-associated changes. They unveil early Alzheimer’s disease CSF-specific proteomic signatures and potential therapeutic targets.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 10","pages":"2125-2141"},"PeriodicalIF":19.4,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145294938","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}
Pub Date : 2025-10-09DOI: 10.1038/s43587-025-00991-2
Using genome-wide analyses in over 56,000 individuals, we identify 59 genetic loci linked to brain aging, of which 39 are novel. This work also uncovers key biological pathways that connect brain aging to mental, metabolic, cardiovascular and lifestyle factors, and offers insights for promoting healthy aging and preventing neurodegenerative diseases.
{"title":"New genetic insights show how modifiable risk factors influence brain aging","authors":"","doi":"10.1038/s43587-025-00991-2","DOIUrl":"10.1038/s43587-025-00991-2","url":null,"abstract":"Using genome-wide analyses in over 56,000 individuals, we identify 59 genetic loci linked to brain aging, of which 39 are novel. This work also uncovers key biological pathways that connect brain aging to mental, metabolic, cardiovascular and lifestyle factors, and offers insights for promoting healthy aging and preventing neurodegenerative diseases.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 10","pages":"1942-1943"},"PeriodicalIF":19.4,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145260363","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}
Within each cell, metabolite-sensing factors respond to coordinate metabolic homeostasis. How metabolic homeostasis is regulated intercellularly and how this may become dysregulated with age, however, remains underexplored. Here we describe a system regulated by a metabolite sensor, CtBP2. CtBP2 is secreted via exosomes in response to reductive metabolism, which is suppressed by oxidative stress. Exosomal CtBP2 administration extends lifespan in aged mice and improves healthspan in particular by reducing frailty. Mechanistically, we identify activation of CYB5R3 and AMPK downstream of exosomal CtBP2. Consistently, serum CtBP2 levels decrease with age and are negatively associated with cardiovascular disease incidence in humans yet are elevated in individuals from families with a history of longevity. Together our findings define a CtBP2-mediated metabolic system with potential for future clinical applications. Sekiya and colleagues identify that, in response to reductive metabolism, CtBP2 is secreted via exosomes and regulates metabolism in recipient cells via CYB5R3 and AMPK. Exosomal CtBP2 administration extends lifespan and healthspan in aged mice, and serum levels of CtBP2 decline with age in humans.
{"title":"The secreted metabolite sensor CtBP2 links metabolism to healthy lifespan","authors":"Motohiro Sekiya, Kenta Kainoh, Wanpei Chen, Daichi Yamazaki, Tomomi Tsuyuzaki, Yuto Kobari, Ayumi Nakata, Kenji Saito, Nao Aono-Soma, Ali Majid, Hiroshi Ohno, Takafumi Miyamoto, Takashi Matsuzaka, Rikako Nakajima, Takaaki Matsuda, Yuki Murayama, Yoko Sugano, Yoshinori Osaki, Hitoshi Iwasaki, Hitoshi Shimano","doi":"10.1038/s43587-025-00973-4","DOIUrl":"10.1038/s43587-025-00973-4","url":null,"abstract":"Within each cell, metabolite-sensing factors respond to coordinate metabolic homeostasis. How metabolic homeostasis is regulated intercellularly and how this may become dysregulated with age, however, remains underexplored. Here we describe a system regulated by a metabolite sensor, CtBP2. CtBP2 is secreted via exosomes in response to reductive metabolism, which is suppressed by oxidative stress. Exosomal CtBP2 administration extends lifespan in aged mice and improves healthspan in particular by reducing frailty. Mechanistically, we identify activation of CYB5R3 and AMPK downstream of exosomal CtBP2. Consistently, serum CtBP2 levels decrease with age and are negatively associated with cardiovascular disease incidence in humans yet are elevated in individuals from families with a history of longevity. Together our findings define a CtBP2-mediated metabolic system with potential for future clinical applications. Sekiya and colleagues identify that, in response to reductive metabolism, CtBP2 is secreted via exosomes and regulates metabolism in recipient cells via CYB5R3 and AMPK. Exosomal CtBP2 administration extends lifespan and healthspan in aged mice, and serum levels of CtBP2 decline with age in humans.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 11","pages":"2197-2214"},"PeriodicalIF":19.4,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145254386","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}
Aging is characterized by the progressive deterioration of tissue structure and function, leading to increased vulnerability to diseases. Senescent cells (SCs) accumulate with age, but how the immune system regulates their burden is unclear. Here we show that CD4 T cells differentiate into Eomesodermin (Eomes)+CCL5+ T lymphocytes (CD4-Eomes) in a SC-rich environment and that a reduction in the SC load, achieved using senolytic drugs, was sufficient to halt this differentiation. We further demonstrate that eliminating CD4-Eomes cells at advanced age by selectively deleting the Eomes transcription factor in CD4 T cells results in increased accumulation of SCs, profound physical deterioration and a decreased lifespan. In liver cirrhosis, a model of localized chronic inflammation, CD4-Eomes cell elimination increased fibrosis, SC load and worsened the disease. Collectively, our findings demonstrate the fundamental role of CD4-Eomes cells in modulating tissue senescence, with implications for age-related diseases and longevity. Elyahu and colleagues describe the reciprocal interplay between senescent cells (SCs) and a helper T cell population that accumulates during aging. They show that selective depletion of this T cell population increases SC accumulation, accelerates frailty and limits lifespan in mice.
{"title":"CD4 T cells acquire Eomesodermin to modulate cellular senescence and aging","authors":"Yehezqel Elyahu, Ilana Feygin, Ekaterina Eremenko, Noa Pinkas, Alon Zemer, Amit Shicht, Omer Berner, Roni Avigdory-Meiri, Anna Nemirovsky, Keren Reshef, Lior Roitman, Valery Krizhanovsky, Alon Monsonego","doi":"10.1038/s43587-025-00953-8","DOIUrl":"10.1038/s43587-025-00953-8","url":null,"abstract":"Aging is characterized by the progressive deterioration of tissue structure and function, leading to increased vulnerability to diseases. Senescent cells (SCs) accumulate with age, but how the immune system regulates their burden is unclear. Here we show that CD4 T cells differentiate into Eomesodermin (Eomes)+CCL5+ T lymphocytes (CD4-Eomes) in a SC-rich environment and that a reduction in the SC load, achieved using senolytic drugs, was sufficient to halt this differentiation. We further demonstrate that eliminating CD4-Eomes cells at advanced age by selectively deleting the Eomes transcription factor in CD4 T cells results in increased accumulation of SCs, profound physical deterioration and a decreased lifespan. In liver cirrhosis, a model of localized chronic inflammation, CD4-Eomes cell elimination increased fibrosis, SC load and worsened the disease. Collectively, our findings demonstrate the fundamental role of CD4-Eomes cells in modulating tissue senescence, with implications for age-related diseases and longevity. Elyahu and colleagues describe the reciprocal interplay between senescent cells (SCs) and a helper T cell population that accumulates during aging. They show that selective depletion of this T cell population increases SC accumulation, accelerates frailty and limits lifespan in mice.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 10","pages":"1970-1982"},"PeriodicalIF":19.4,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145246046","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}
Pub Date : 2025-10-06DOI: 10.1038/s43587-025-00983-2
Michael S. Ringel, Yue Zhang, Wen Kin Lim
{"title":"Accelerating activity in the longevity biopharmaceutical sector","authors":"Michael S. Ringel, Yue Zhang, Wen Kin Lim","doi":"10.1038/s43587-025-00983-2","DOIUrl":"10.1038/s43587-025-00983-2","url":null,"abstract":"","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 12","pages":"2357-2358"},"PeriodicalIF":19.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145240713","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}
Pub Date : 2025-10-06DOI: 10.1038/s43587-025-00988-x
Joe Swift, Angela Cucchi, Michael Chang, Richard G. A. Faragher, Carol A. Holland, Itziar Tueros, Matthew J. Dalby, Elizabeth G. Canty-Laird
On 12 February 2025, a joint meeting of the UK Aging Networks was held in Liverpool, UK. It was convened by the ECMage (extracellular matrix aging) network and EuroAgeNet, an initiative led by ECMage but involving four other UK aging networks — namely, the building links in aging science and translation network (BLAST), the cognitive frailty interdisciplinary network (CFIN), the aging and nutrient sensing network (AGENTS) and the food systems for older people (Food4Years) network — together with industrial and European partners. In this Meeting Report, we summarize the opinions of an industrial panel and round-table discussions on barriers and opportunities related to academic–industrial partnerships.
{"title":"Considerations for creating effective academic–industrial partnerships","authors":"Joe Swift, Angela Cucchi, Michael Chang, Richard G. A. Faragher, Carol A. Holland, Itziar Tueros, Matthew J. Dalby, Elizabeth G. Canty-Laird","doi":"10.1038/s43587-025-00988-x","DOIUrl":"10.1038/s43587-025-00988-x","url":null,"abstract":"On 12 February 2025, a joint meeting of the UK Aging Networks was held in Liverpool, UK. It was convened by the ECMage (extracellular matrix aging) network and EuroAgeNet, an initiative led by ECMage but involving four other UK aging networks — namely, the building links in aging science and translation network (BLAST), the cognitive frailty interdisciplinary network (CFIN), the aging and nutrient sensing network (AGENTS) and the food systems for older people (Food4Years) network — together with industrial and European partners. In this Meeting Report, we summarize the opinions of an industrial panel and round-table discussions on barriers and opportunities related to academic–industrial partnerships.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 11","pages":"2153-2157"},"PeriodicalIF":19.4,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145240747","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}
Pub Date : 2025-10-03DOI: 10.1038/s43587-025-00989-w
Nektarios Tavernarakis
Bai and colleagues show that specialized translation hubs called mitochondria-associated translation organelles (MATOs) form by liquid–liquid phase separation on the mitochondrial surface. MATOs congregate ribosomes and specific mRNAs to supply key proteins on-site and thereby uphold mitochondrial integrity and function. Persistent association of MATOs with mitochondria enhances stress resistance and extends lifespan.
{"title":"Phase separation meets energy generation to boost longevity","authors":"Nektarios Tavernarakis","doi":"10.1038/s43587-025-00989-w","DOIUrl":"10.1038/s43587-025-00989-w","url":null,"abstract":"Bai and colleagues show that specialized translation hubs called mitochondria-associated translation organelles (MATOs) form by liquid–liquid phase separation on the mitochondrial surface. MATOs congregate ribosomes and specific mRNAs to supply key proteins on-site and thereby uphold mitochondrial integrity and function. Persistent association of MATOs with mitochondria enhances stress resistance and extends lifespan.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 10","pages":"1936-1938"},"PeriodicalIF":19.4,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145226540","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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