Nature aging最新文献_第7页

Dietary patterns and accelerated multimorbidity in older adults 老年人的饮食模式和加速多发病。

IF 19.4

Nature aging Pub Date : 2025-07-28 DOI: 10.1038/s43587-025-00929-8

David Abbad-Gomez, Adrián Carballo-Casla, Giorgi Beridze, Esther Lopez-Garcia, Fernando Rodríguez-Artalejo, Maria Sala, Mercè Comas, Davide Liborio Vetrano, Amaia Calderón-Larrañaga

{"title":"Dietary patterns and accelerated multimorbidity in older adults","authors":"David Abbad-Gomez, Adrián Carballo-Casla, Giorgi Beridze, Esther Lopez-Garcia, Fernando Rodríguez-Artalejo, Maria Sala, Mercè Comas, Davide Liborio Vetrano, Amaia Calderón-Larrañaga","doi":"10.1038/s43587-025-00929-8","DOIUrl":"10.1038/s43587-025-00929-8","url":null,"abstract":"Diet could influence disease development and shape multimorbidity trajectories. Here we examined how four dietary patterns relate to 15-year multimorbidity accumulation in 2,473 community-dwelling older adults from the Swedish SNAC-K cohort. Multimorbidity was operationalized as the total number of chronic conditions and grouped into three organ systems. Higher adherence to the Mediterranean-DASH Diet Intervention for Neurodegenerative Delay, the Alternative Healthy Eating Index and the Alternative Mediterranean Diet was inversely associated with the annual rate of total chronic disease accumulation (β coefficient (95% confidence interval) per 1-s.d. increment: −0.049 (−0.065 to −0.032), −0.051 (−0.068 to −0.035) and −0.031 (−0.048 to −0.014), respectively), whereas higher adherence to the Empirical Dietary Inflammatory Index was associated with a faster rate of accumulation (0.053 (0.035–0.071)). Similar associations were observed for cardiovascular and neuropsychiatric diseases but not for musculoskeletal diseases. Some associations varied by sex and age. Our findings support diet quality as a modifiable risk factor for multimorbidity progression in older adults, with possible implications for dietary guidelines, public health strategies and clinical practice. In a Swedish cohort, Abbad-Gomez et al. report that diet quality is inversely associated with the rate of accumulation of total, cardiovascular and neuropsychiatric chronic diseases in older adults, supporting diet quality as a modifiable risk factor for multimorbidity progression.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 8","pages":"1481-1490"},"PeriodicalIF":19.4,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12350159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144736444","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

Inflammation sends old muscle stem cells into a rusty meltdown 炎症会使老化的肌肉干细胞生锈。

IF 19.4

Nature aging Pub Date : 2025-07-25 DOI: 10.1038/s43587-025-00937-8

Ohanes Ashekyan, Michael A. Rudnicki

引用次数: 0

Lifestyle interventions can save over US $500 million in healthcare spending 生活方式干预可以节省5亿多美元的医疗保健支出。

IF 19.4

Nature aging Pub Date : 2025-07-17 DOI: 10.1038/s43587-025-00916-z

引用次数: 0

The GNPC provides a proteomic resource for biomarker discovery and mechanistic insight in neurodegenerative disease GNPC为神经退行性疾病的生物标志物发现和机制洞察提供了蛋白质组学资源。

IF 19.4

Nature aging Pub Date : 2025-07-15 DOI: 10.1038/s43587-025-00920-3

Simon Lovestone, Farhad Imam, on behalf of the Global Neurodegeneration Proteomics Consortium (GNPC) Scientific Steering Committee

引用次数: 0

Disease burden, lifetime healthcare cost and long-term intervention impact projections among older adults in Singapore 新加坡老年人的疾病负担、终生医疗保健费用和长期干预影响预测。

IF 19.4

Nature aging Pub Date : 2025-07-15 DOI: 10.1038/s43587-025-00915-0

Xueying Guo, Bryan Tysinger, Hwee Lin Wee, Mythily Subramaniam, Stefan Ma, Tze Pin Ng, Cynthia Chen

{"title":"Disease burden, lifetime healthcare cost and long-term intervention impact projections among older adults in Singapore","authors":"Xueying Guo, Bryan Tysinger, Hwee Lin Wee, Mythily Subramaniam, Stefan Ma, Tze Pin Ng, Cynthia Chen","doi":"10.1038/s43587-025-00915-0","DOIUrl":"10.1038/s43587-025-00915-0","url":null,"abstract":"Singapore’s rapidly aging population and increasing healthcare demands highlight the need for projections to inform policy planning. Here we adapted a previously published dynamic Markov microsimulation model, the Future Elderly Model, to estimate disease trajectories and healthcare expenditure among adults aged 51 years and older in Singapore. The model simulated four long-term lifestyle interventions aligned with the Healthier SG program from 2020 to 2050. Our projections indicate an increasing prevalence of chronic conditions, comorbidities, obesity and disabilities, with ethnic differences. The projected lifetime healthcare expenditure is the highest among Indians (US $93,900; 95% credible interval (CI), US $68,900–119,000), followed by the Chinese (US $75,700; 95% CI, US $57,600–93,800) and Malays (US $70,000; 95% CI, US $52,000–88,000). Despite having a higher chronic disease burden, Malays are expected to incur lower lifetime expenditure due to their shorter life expectancy. Implementing all 4 interventions could save US $505 million (95% CI, US $462–547 million) in healthcare use by 2050. Sustained lifestyle interventions may moderate the increase in future burdens. Policy strategies should prioritize preventive care tailored to the specific needs of diverse population subgroups. Population aging presents challenges for healthcare and social care systems in ensuring that services are available for older adults. Here the authors performed a Singapore-based simulation study that projects rising chronic disease prevalence and healthcare costs, showing that long-term lifestyle interventions can moderate the increase in future diseases and healthcare spending by 2050.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 7","pages":"1358-1369"},"PeriodicalIF":19.4,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12270899/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144644462","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

Extracellular vesicles from antler blastema progenitor cells reverse bone loss and mitigate aging-related phenotypes in mice and macaques 鹿角胚祖细胞的细胞外囊泡逆转骨质流失并减轻小鼠和猕猴的衰老相关表型。

IF 19.4

Nature aging Pub Date : 2025-07-14 DOI: 10.1038/s43587-025-00918-x

Yiming Hao, Beibei Yu, Mingze Qin, Tao Qin, Jianhong Wang, Yitao Wei, Chengxiang Zhao, Yaowen Xing, Yuan Yuan, Tingfeng Xue, Borui Xue, Yali Zhang, Hongdi Huang, Xiaomei Yu, Yunchao Ji, Minghao Qiu, Yufang Zhou, Bing Xia, Teng Ma, Shengyou Li, Haining Wu, Xue Gao, Yujie Yang, Lingli Guo, Yongfeng Zhang, Zhenguo Wang, Huiling Sun, Xueli Gao, Zujian Huang, Longbao Lv, Dongdong Wu, Zhipeng Li, Yonggang Yao, Wen Wang, Zhuojing Luo, Qiang Qiu, Jinghui Huang

{"title":"Extracellular vesicles from antler blastema progenitor cells reverse bone loss and mitigate aging-related phenotypes in mice and macaques","authors":"Yiming Hao, Beibei Yu, Mingze Qin, Tao Qin, Jianhong Wang, Yitao Wei, Chengxiang Zhao, Yaowen Xing, Yuan Yuan, Tingfeng Xue, Borui Xue, Yali Zhang, Hongdi Huang, Xiaomei Yu, Yunchao Ji, Minghao Qiu, Yufang Zhou, Bing Xia, Teng Ma, Shengyou Li, Haining Wu, Xue Gao, Yujie Yang, Lingli Guo, Yongfeng Zhang, Zhenguo Wang, Huiling Sun, Xueli Gao, Zujian Huang, Longbao Lv, Dongdong Wu, Zhipeng Li, Yonggang Yao, Wen Wang, Zhuojing Luo, Qiang Qiu, Jinghui Huang","doi":"10.1038/s43587-025-00918-x","DOIUrl":"10.1038/s43587-025-00918-x","url":null,"abstract":"Antler blastema progenitor cells (ABPCs) are a distinct population of skeletal mesenchymal stem cells found in regenerating deer antlers, with strong stemness and renewal capacity in vitro. Stem cell-derived extracellular vesicles (EVs) are emerging as potential therapeutic candidates that can mediate donor cells’ beneficial effects. Here, we tested the effects of ABPC-derived EVs (EVsABPC) on aging in mice and rhesus macaques (Macaca mulatta). We identified a variety of unique factors in EVsABPC and showed that in vitro, EVsABPC attenuated phenotypes of senescence in bone marrow stem cells. In aged mice and macaques, EVsABPC substantially increased femoral bone mineral density. Further, intravenous EVsABPC improved physical performance, enhanced cognitive function and reduced systemic inflammation in aged mice, while reversing epigenetic age by over 3 months. In macaques, EVABPC treatment was also neuroprotective, reduced inflammation, improved locomotor function and reduced epigenetic age by over 2 years. Our findings position ABPCs as an emerging and practical source of EVs with translational value for healthy aging interventions. Inspired by the regenerative capacity of deer antlers, Hao and colleagues report that antler blastema progenitor cell-derived extracellular vesicle treatment counteracts bone loss and epigenetic aging and is neuroprotective in mice and macaques.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 9","pages":"1790-1809"},"PeriodicalIF":19.4,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12443635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144639140","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

Rethinking inflammaging across human diversity 重新思考人类多样性的炎症。

IF 19.4

Nature aging Pub Date : 2025-07-14 DOI: 10.1038/s43587-025-00933-y

Marina Terekhova, Maxim Artyomov

引用次数: 0

Single-cell and spatial transcriptomics map senescent vascular cells in arterial remodeling during atherosclerosis in mice 单细胞和空间转录组学绘制小鼠动脉粥样硬化期间动脉重塑中的衰老血管细胞。

IF 19.4

Nature aging Pub Date : 2025-07-14 DOI: 10.1038/s43587-025-00889-z

Krystyna Mazan-Mamczarz, Dimitrios Tsitsipatis, Bennett G. Childs, Angelica E. Carr, Carla Rocha Dos Santos, Carlos Anerillas, Brigette Romero, Jordan M. Gregg, Charnae’ Henry-Smith, Ada N. Okereke, Marc Michel, Rachel Munk, Jennifer L. Martindale, Yulan Piao, Jinshui Fan, Maria O. Hernandez, Noemi Kedei, Michael L. Viacheslavov, Madeline M. F. Wong, Olga V. Fedorova, Mona Batish, Supriyo De, Darren J. Baker, Myriam Gorospe, Allison B. Herman

{"title":"Single-cell and spatial transcriptomics map senescent vascular cells in arterial remodeling during atherosclerosis in mice","authors":"Krystyna Mazan-Mamczarz, Dimitrios Tsitsipatis, Bennett G. Childs, Angelica E. Carr, Carla Rocha Dos Santos, Carlos Anerillas, Brigette Romero, Jordan M. Gregg, Charnae’ Henry-Smith, Ada N. Okereke, Marc Michel, Rachel Munk, Jennifer L. Martindale, Yulan Piao, Jinshui Fan, Maria O. Hernandez, Noemi Kedei, Michael L. Viacheslavov, Madeline M. F. Wong, Olga V. Fedorova, Mona Batish, Supriyo De, Darren J. Baker, Myriam Gorospe, Allison B. Herman","doi":"10.1038/s43587-025-00889-z","DOIUrl":"10.1038/s43587-025-00889-z","url":null,"abstract":"Growing evidence suggests that the induction of cellular senescence in vascular cells is causally linked to the etiology of cardiovascular diseases. To investigate systematically the heterogeneity of senescent vascular cells in atherosclerosis, we used a high-fat diet and PCSK9 overexpression to induce atherosclerosis in a senescence reporter mouse model (p16-tdTomato+/−) and performed single-cell RNA sequencing on whole aortas. Using the SenMayo and CellAge gene sets, we identified four clusters of vascular smooth muscle cells (VSMCs), fibroblasts and T cells enriched in features of senescence, which were reduced upon treatment with the senolytic agent ABT-737. We then derived a global senescence signature of atherosclerosis including Spp1, Ctsb and Tnfrsf11b mRNAs. We validated the enrichment of these mRNAs in senescence by using spatial transcriptomics in a second mouse model of atherosclerosis and senolysis (Ldlr−/−; p16-3MR), as well as by analyzing in vitro models of human VSMC senescence. Our results uncover a vascular-specific transcriptomic signature of senescence that may be exploited for tracking and treating age-related vascular diseases. Mazan-Mamczarz, Tsitsipatis and colleagues apply single-cell and spatial transcriptomics to mouse models of atherosclerosis to map senescent cells contributing to plaque instability and arterial remodeling. They define a transcriptomic signature of vascular senescence.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 8","pages":"1528-1547"},"PeriodicalIF":19.4,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144639142","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

Characterizing primary and secondary senescence in vivo 体内原发性和继发性衰老的特征。

IF 19.4

Nature aging Pub Date : 2025-07-11 DOI: 10.1038/s43587-025-00917-y

Yuko Sogabe, Hirofumi Shibata, Mio Kabata, Akito Tanaka, Kanae Mitsunaga, Kazunori Sunadome, May Nakajima-Koyama, Michitada Hirano, Eisuke Nishida, Knut Woltjen, Hiroshi Seno, Yasuhiro Yamada, Takuya Yamamoto

{"title":"Characterizing primary and secondary senescence in vivo","authors":"Yuko Sogabe, Hirofumi Shibata, Mio Kabata, Akito Tanaka, Kanae Mitsunaga, Kazunori Sunadome, May Nakajima-Koyama, Michitada Hirano, Eisuke Nishida, Knut Woltjen, Hiroshi Seno, Yasuhiro Yamada, Takuya Yamamoto","doi":"10.1038/s43587-025-00917-y","DOIUrl":"10.1038/s43587-025-00917-y","url":null,"abstract":"There is robust evidence that senescence can be propagated in vitro through mechanisms including the senescence-associated secretory phenotype, resulting in the non-cell-autonomous induction of secondary senescence. However, the induction, regulation and physiological role of secondary senescence in vivo remain largely unclear. Here we generated senescence-inducible mouse models expressing either the constitutively active form of MEK1 or MKK6 and mCherry, to map primary and secondary senescent cells. Our models recapitulate characteristic features of senescence and demonstrate that primary and secondary phenotypes are highly tissue- and inducer-dependent. Spatially resolved RNA expression analyses at the single-cell level reveal that each senescence induction results in a unique transcriptional profile—even within cells of the same cell type—explaining the heterogeneity of senescent cells in vivo. Furthermore, we show that interleukin-1β, primarily derived from macrophages, induces secondary phenotypes. Our findings provide insight into secondary senescence in vivo and useful tools for understanding and manipulating senescence during aging. Through non-cell-autonomous functions, senescent cells can induce secondary senescence in bystander cells. Sogabe et al. generate mouse models of MEK1- or MKK6-induced senescence and use double labeling to map primary and secondary senescence in vivo using single-cell and spatial analysis.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 8","pages":"1568-1588"},"PeriodicalIF":19.4,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621631","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

Author Correction: mRNA metabolism regulator human antigen R (HuR) regulates age-related hearing loss in aged mice 作者更正：mRNA代谢调节剂人抗原R （HuR）调节老年小鼠的年龄相关性听力损失。

IF 19.4

Nature aging Pub Date : 2025-07-08 DOI: 10.1038/s43587-025-00936-9

Siwei Guo, Jieying Cao, Guodong Hong, Yuning Song, Ming Xia, Peipei Li, Wei Yuan, Yu Xiao, Guoqiang Sun, Shuang Liu, Shengda Cao, Jieyu Qi, Xiuli Bi, Ziyi Liu, Yunhao Wu, Wen Li, Xiaoxu Zhao, Jiangang Gao, Renjie Chai, Xiaolong Fu

引用次数: 0