Nature aging最新文献_第3页

Promoting health and survival through lowered body temperature. 通过降低体温促进健康和生存。

IF 17

Nature aging Pub Date : 2025-04-09 DOI: 10.1038/s43587-025-00850-0

Bruno Conti, Rafael de Cabo

{"title":"Promoting health and survival through lowered body temperature.","authors":"Bruno Conti, Rafael de Cabo","doi":"10.1038/s43587-025-00850-0","DOIUrl":"https://doi.org/10.1038/s43587-025-00850-0","url":null,"abstract":"Core body temperature (Tb) is a long-established determinant of longevity across species. In this Perspective, we first summarize evidence demonstrating that reducing Tb increases lifespan and that lowered Tb contributes to the antiaging effects of calorie restriction. Next, we discuss recent data that diverge from prior hypotheses on the mechanisms by which Tb affects longevity, suggesting these are limited neither to the thermodynamics of nonenzymatic chemical reactions, nor reduced formation of mitochondrial reactive oxygen species nor lowered metabolic rate. Instead, recent findings in invertebrates show that cold promotes longevity via specific pathways including nutrient sensing and proteostasis, as well as modulating the thermodynamics of proteins and nucleic acids by changing their structure and function, for example, affecting temperature-sensitive ion channels, long-lived temperature-sensitive dauer mutations, base-pair stability and stem-loop RNA structures. Temperature affects the epigenetic signature and inflammation, and lowering Tb can also induce RNA-binding cold shock proteins, activate cold-sensitive kinases and differential splicing to potentially reshape the cellular environment. Finally, we reflect on important future work and the translational potential of temperature management and temperature mimetics.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":17.0,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144061077","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}

引用次数: 0

The effect of ambient air pollution (PM_2.5) on dementia risk. 环境空气污染（PM2.5）对痴呆风险的影响。

IF 17

Nature aging Pub Date : 2025-04-09 DOI: 10.1038/s43587-025-00865-7

引用次数: 0

Regeneration leads to global tissue rejuvenation in aging sexual planarians. 再生导致老龄性涡虫的整体组织年轻化。

IF 17

Nature aging Pub Date : 2025-04-03 DOI: 10.1038/s43587-025-00847-9

Xiaoting Dai, Xinghua Li, Alexander Tyshkovskiy, Cassandra Zuckerman, Nan Cheng, Peter Lin, David Paris, Saad Qureshi, Leonid Kruglyak, Xiaoming Mao, Jayakrishnan Nandakumar, Vadim N Gladyshev, Scott Pletcher, Jacob Sobota, Longhua Guo

{"title":"Regeneration leads to global tissue rejuvenation in aging sexual planarians.","authors":"Xiaoting Dai, Xinghua Li, Alexander Tyshkovskiy, Cassandra Zuckerman, Nan Cheng, Peter Lin, David Paris, Saad Qureshi, Leonid Kruglyak, Xiaoming Mao, Jayakrishnan Nandakumar, Vadim N Gladyshev, Scott Pletcher, Jacob Sobota, Longhua Guo","doi":"10.1038/s43587-025-00847-9","DOIUrl":"10.1038/s43587-025-00847-9","url":null,"abstract":"The possibility of reversing the adverse impacts of aging could significantly reduce age-related diseases and improve quality of life in older populations. Here we report that the sexual lineage of the planarian Schmidtea mediterranea exhibits physiological decline within 18 months of birth, including altered tissue architecture, impaired fertility and motility, and increased oxidative stress. Single-cell profiling of young and older planarian heads uncovered loss of neurons and muscle, increase of glia, and revealed minimal changes in somatic pluripotent stem cells, along with molecular signatures of aging across tissues. Remarkably, amputation followed by regeneration of lost tissues in older planarians led to reversal of these age-associated changes in tissues both proximal and distal to the injury at physiological, cellular and molecular levels. Our work suggests mechanisms of rejuvenation in both new and old tissues concurring with planarian regeneration, which may provide valuable insights for antiaging interventions.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":17.0,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782202","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}

引用次数: 0

The advantages and challenges of disability-free survival as outcome measure in clinical studies. 无残疾生存在临床研究中的优势和挑战。

IF 17

Nature aging Pub Date : 2025-04-01 DOI: 10.1038/s43587-025-00853-x

Johannes T Neumann, John J McNeil

引用次数: 0

Interplay of somatic mutations and epigenetic aging clocks. 体细胞突变与表观遗传衰老时钟的相互作用。

IF 17

Nature aging Pub Date : 2025-04-01 DOI: 10.1038/s43587-025-00846-w

Wolfgang Wagner

引用次数: 0

Somatic mutation as an explanation for epigenetic aging. 体细胞突变是表观遗传衰老的一种解释。

IF 17

Nature aging Pub Date : 2025-04-01 Epub Date: 2025-01-13 DOI: 10.1038/s43587-024-00794-x

Zane Koch, Adam Li, Daniel S Evans, Steven Cummings, Trey Ideker

引用次数: 0

FGF21 keeps the thymus young. FGF21使胸腺保持年轻。

IF 17

Nature aging Pub Date : 2025-04-01 DOI: 10.1038/s43587-025-00814-4

Yousuke Takahama

引用次数: 0

Alarmingly large care deficits globally for people living with dementia and disability. 全球对痴呆症和残疾患者的护理缺口惊人。

IF 17

Nature aging Pub Date : 2025-04-01 DOI: 10.1038/s43587-025-00849-7

引用次数: 0

Paracrine FGF21 dynamically modulates mTOR signaling to regulate thymus function across the lifespan. 旁分泌FGF21动态调节mTOR信号，调节胸腺功能。

IF 17

Nature aging Pub Date : 2025-04-01 Epub Date: 2025-02-19 DOI: 10.1038/s43587-024-00801-1

Sarah A Wedemeyer, Nicholas E Jones, Iwan G A Raza, Freedom M Green, Yangming Xiao, Manpreet K Semwal, Aaron K Garza, Kahealani S Archuleta, Kymberly L Wimberly, Thomas Venables, Georg A Holländer, Ann V Griffith

{"title":"Paracrine FGF21 dynamically modulates mTOR signaling to regulate thymus function across the lifespan.","authors":"Sarah A Wedemeyer, Nicholas E Jones, Iwan G A Raza, Freedom M Green, Yangming Xiao, Manpreet K Semwal, Aaron K Garza, Kahealani S Archuleta, Kymberly L Wimberly, Thomas Venables, Georg A Holländer, Ann V Griffith","doi":"10.1038/s43587-024-00801-1","DOIUrl":"10.1038/s43587-024-00801-1","url":null,"abstract":"Consequences of age-associated thymic atrophy include declining T-cell responsiveness to pathogens and vaccines and diminished T-cell self-tolerance. Cortical thymic epithelial cells (cTECs) are primary targets of thymic aging, and recent studies suggested that their maintenance requires mTOR signaling downstream of medullary TEC (mTEC)-derived growth factors. Here, to test this hypothesis, we generated a knock-in mouse model in which FGF21 and mCherry are expressed by most mTECs. We find that mTEC-derived FGF21 promotes temporally distinct patterns of mTORC1 and mTORC2 signaling in cTECs, promotes thymus and individual cTEC growth and maintenance, increases T-cell responsiveness to viral infection, and diminishes indicators of peripheral autoimmunity in older mice. The effects of FGF21 overexpression on thymus size and mTOR signaling were abrogated by treatment with the mTOR inhibitor rapamycin. These results reveal a mechanism by which paracrine FGF21 signaling regulates thymus size and function throughout the lifespan, as well as potential therapeutic targets for improving T-cell function and tolerance in aging.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":"588-606"},"PeriodicalIF":17.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12003089/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460848","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}

引用次数: 0

Niche-derived Semaphorin 4A safeguards functional identity of myeloid-biased hematopoietic stem cells. 小生境衍生的信号蛋白4A保护骨髓偏向性造血干细胞的功能特性。

IF 17

Nature aging Pub Date : 2025-04-01 Epub Date: 2025-01-29 DOI: 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":"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.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":"558-575"},"PeriodicalIF":17.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12025894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143070472","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}

引用次数: 0