Nature aging最新文献_第7页

Oligodendrocyte ankyrin G in aging 少突胶质细胞锚定蛋白G在衰老中的作用。

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Nature aging Pub Date : 2025-02-12 DOI: 10.1038/s43587-025-00826-0

George Andrew S. Inglis

引用次数: 0

Effect of cholinergic modulator in Parkinson’s disease with cognitive impairment 胆碱能调节剂在帕金森病伴认知障碍中的作用。

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Nature aging Pub Date : 2025-02-10 DOI: 10.1038/s43587-025-00825-1

Yahyah Aman

引用次数: 0

Recommendations for implementing the Hevolution Alliance for Aging Biomarkers initiative 实施老化生物标志物进化联盟倡议的建议。

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Nature aging Pub Date : 2025-02-06 DOI: 10.1038/s43587-025-00812-6

Toshiko Tanaka, Felipe Sierra, Vadim N. Gladyshev, Tony Wyss-Coray, Ana Maria Cuervo, Viviana Perez, Luigi Ferrucci, On behalf of the Hevolution Alliance for Aging Biomarkers

引用次数: 0

Multiomics atlas reveals molecular and genetic drivers of human ovarian aging 多组学图谱揭示了人类卵巢衰老的分子和遗传驱动因素。

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Nature aging Pub Date : 2025-02-05 DOI: 10.1038/s43587-025-00821-5

引用次数: 0

Transdisciplinary links between societal inequality and brain structure and dynamics 社会不平等与大脑结构和动态之间的跨学科联系。

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Nature aging Pub Date : 2025-02-05 DOI: 10.1038/s43587-025-00822-4

引用次数: 0

Multi-omic profiling of sarcopenia identifies disrupted branched-chain amino acid catabolism as a causal mechanism and therapeutic target 肌少症的多组学分析确定了中断的支链氨基酸分解代谢是一种因果机制和治疗靶点。

IF 17

Nature aging Pub Date : 2025-02-05 DOI: 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}

引用次数: 0

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 在DO-HEALTH试验中，维生素D、omega-3和运动对老年人生物衰老的DNA甲基化时钟的个体和累加效应。

IF 17

Nature aging Pub Date : 2025-02-03 DOI: 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}

引用次数: 0

A BCL-xL/BCL-2 PROTAC effectively clears senescent cells in the liver and reduces MASH-driven hepatocellular carcinoma in mice BCL-xL/BCL-2 PROTAC可有效清除小鼠肝脏中的衰老细胞并减少mash驱动的肝细胞癌。

IF 17

Nature aging Pub Date : 2025-01-31 DOI: 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}

引用次数: 0

Author Correction: Generation of a selective senolytic platform using a micelle-encapsulated Sudan Black B conjugated analog 作者更正：使用胶束封装的苏丹黑B共轭类似物产生选择性衰老平台。

IF 17

Nature aging Pub Date : 2025-01-31 DOI: 10.1038/s43587-025-00820-6

Sophia Magkouta, Dimitris Veroutis, Angelos Papaspyropoulos, Maria Georgiou, Nikolaos Lougiakis, Natassa Pippa, Sophia Havaki, Anastasia Palaiologou, Dimitris-Foivos Thanos, Konstantinos Kambas, Nefeli Lagopati, Nikos Boukos, Nicole Pouli, Panagiotis Marakos, Athanassios Kotsinas, Dimitris Thanos, Konstantinos Evangelou, Fotios Sampaziotis, Constantin Tamvakopoulos, Stergios Pispas, Russell Petty, Nicholas Kotopoulos, Vassilis G. Gorgoulis

引用次数: 0

Ginkgolide B increases healthspan and lifespan of female mice 银杏内酯B增加雌性小鼠的健康寿命和寿命。

IF 17

Nature aging Pub Date : 2025-01-31 DOI: 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}

引用次数: 0