Nature aging最新文献_第8页

Author Correction: Heterochronic parabiosis reprograms the mouse brain transcriptome by shifting aging signatures in multiple cell types 作者更正：异慢性异种共生通过改变多种细胞类型的衰老特征来重编程小鼠脑转录组。

IF 17

Nature aging Pub Date : 2025-01-29 DOI: 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

引用次数: 0

Transposable element methylation tracks age 转座因子甲基化与年龄有关。

IF 17

Nature aging Pub Date : 2025-01-27 DOI: 10.1038/s43587-025-00807-3

Bernadette Hotzi, Tibor Vellai

引用次数: 0

Menopause-induced 17β-estradiol and progesterone loss increases senescence markers, matrix disassembly and degeneration in mouse cartilage 绝经诱导的17β-雌二醇和黄体酮损失增加了小鼠软骨的衰老标志物、基质解体和变性

IF 17

Nature aging Pub Date : 2025-01-16 DOI: 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}

引用次数: 0

Aging stem cells limit tumorigenesis 衰老的干细胞限制肿瘤的发生

IF 17

Nature aging Pub Date : 2025-01-15 DOI: 10.1038/s43587-025-00805-5

Yahyah Aman

引用次数: 0

GD3 ganglioside checkpoints in immune surveillance of senescent cells 衰老细胞免疫监测中的GD3神经节苷脂检查点。

IF 17

Nature aging Pub Date : 2025-01-15 DOI: 10.1038/s43587-025-00803-7

Julia Majewska, Valery Krizhanovsky

引用次数: 0

Semaglutide alleviates knee osteoarthritis pain in persons with obesity 西马鲁肽减轻肥胖患者膝骨关节炎疼痛。

IF 17

Nature aging Pub Date : 2025-01-14 DOI: 10.1038/s43587-025-00809-1

Yahyah Aman

引用次数: 0

Unequal life expectancy across ten Americas 十个美洲的平均寿命不平等。

IF 17

Nature aging Pub Date : 2025-01-14 DOI: 10.1038/s43587-025-00806-4

George Andrew S. Inglis

引用次数: 0

Publisher Correction: Cohort trends in intrinsic capacity in England and China 出版者更正：英国和中国内在能力的队列趋势。

IF 17

Nature aging Pub Date : 2025-01-13 DOI: 10.1038/s43587-025-00808-2

John R. Beard, Katja Hanewald, Yafei Si, Jotheeswaran Amuthavalli Thiyagarajan, Dario Moreno-Agostino

引用次数: 0

Gut microbial-derived phenylacetylglutamine accelerates host cellular senescence 肠道微生物衍生的苯乙酰谷氨酰胺加速宿主细胞衰老。

IF 17

Nature aging Pub Date : 2025-01-10 DOI: 10.1038/s43587-024-00795-w

Hao Yang, Tongyao Wang, Chenglang Qian, Huijing Wang, Dong Yu, Meifang Shi, Mengwei Fu, Xueguang Liu, Miaomiao Pan, Xingyu Rong, Zhenming Xiao, Xiejiu Chen, Anaguli Yeerken, Yonglin Wu, Yufan Zheng, Hui Yang, Ming Zhang, Tao Liu, Peng Qiao, Yifan Qu, Yong Lin, Yiqin Huang, Jianliang Jin, Nan Liu, Yumei Wen, Ning Sun, Chao Zhao

{"title":"Gut microbial-derived phenylacetylglutamine accelerates host cellular senescence","authors":"Hao Yang, Tongyao Wang, Chenglang Qian, Huijing Wang, Dong Yu, Meifang Shi, Mengwei Fu, Xueguang Liu, Miaomiao Pan, Xingyu Rong, Zhenming Xiao, Xiejiu Chen, Anaguli Yeerken, Yonglin Wu, Yufan Zheng, Hui Yang, Ming Zhang, Tao Liu, Peng Qiao, Yifan Qu, Yong Lin, Yiqin Huang, Jianliang Jin, Nan Liu, Yumei Wen, Ning Sun, Chao Zhao","doi":"10.1038/s43587-024-00795-w","DOIUrl":"10.1038/s43587-024-00795-w","url":null,"abstract":"Gut microbiota plays a crucial role in the host health in the aging process. However, the mechanisms for how gut microbiota triggers cellular senescence and the consequent impact on human aging remain enigmatic. Here we show that phenylacetylglutamine (PAGln), a metabolite linked to gut microbiota, drives host cellular senescence. Our findings indicate that the gut microbiota alters with age, which leads to increased production of phenylacetic acid (PAA) and its downstream metabolite PAGln in older individuals. The PAGln-induced senescent phenotype was verified in both cellular models and mouse models. Further experiments revealed that PAGln induces mitochondrial dysfunction and DNA damage via adrenoreceptor (ADR)–AMP-activated protein kinase (AMPK) signaling. Blockade of ADRs as well as senolytics therapy impede PAGln-induced cellular senescence in vivo, implying potential anti-aging therapies. This combined evidence reveals that PAGln, a naturally occurring metabolite of human gut microbiota, mechanistically accelerates host cellular senescence. Yang et al. show an age-related increase in the microbial-derived metabolite phenylacetylglutamine that drives host cellular senescence by inducing DNA damage and mitochondrial dysfunction via ADR–AMPK signaling.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 3","pages":"401-418"},"PeriodicalIF":17.0,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142967580","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

EBP1 potentiates amyloid β pathology by regulating γ-secretase EBP1通过调节γ-分泌酶增强β淀粉样蛋白病理。

IF 17

Nature aging Pub Date : 2025-01-08 DOI: 10.1038/s43587-024-00790-1

Byeong-Seong Kim, Inwoo Hwang, Hyo Rim Ko, Young Kwan Kim, Hee Jin Kim, Sang Won Seo, Yujung Choi, Sungsu Lim, Yun Kyung Kim, Shuke Nie, Keqiang Ye, Jong-Chan Park, Yunjong Lee, Dong-Gyu Jo, Seung Eun Lee, Daesik Kim, Sung-Woo Cho, Jee-Yin Ahn

{"title":"EBP1 potentiates amyloid β pathology by regulating γ-secretase","authors":"Byeong-Seong Kim, Inwoo Hwang, Hyo Rim Ko, Young Kwan Kim, Hee Jin Kim, Sang Won Seo, Yujung Choi, Sungsu Lim, Yun Kyung Kim, Shuke Nie, Keqiang Ye, Jong-Chan Park, Yunjong Lee, Dong-Gyu Jo, Seung Eun Lee, Daesik Kim, Sung-Woo Cho, Jee-Yin Ahn","doi":"10.1038/s43587-024-00790-1","DOIUrl":"10.1038/s43587-024-00790-1","url":null,"abstract":"The abnormal deposition of amyloid β (Aβ), produced by proteolytic cleavage events of amyloid precursor protein involving the protease γ-secretase and subsequent polymerization into amyloid plaques, plays a key role in the neuropathology of Alzheimer’s disease (AD). Here we show that ErbB3 binding protein 1 (EBP1)/proliferation-associated 2G4 (PA2G4) interacts with presenilin, a catalytic subunit of γ-secretase, inhibiting Aβ production. Mice lacking forebrain Ebp1/Pa2g4 recapitulate the representative phenotypes of late-onset sporadic AD, displaying an age-dependent increase in Aβ deposition, amyloid plaques and cognitive dysfunction. In postmortem brains of patients with AD and 5x-FAD mice, we found that EBP1 is proteolytically cleaved by asparagine endopeptidase at N84 and N204 residues, compromising its inhibitory effect on γ-secretase, increasing Aβ aggregation and neurodegeneration. Accordingly, injection of AAV2-Ebp1 wild-type or an asparagine endopeptidase-uncleavable mutant into the brains of 5x-FAD mice decreased Aβ generation and alleviated the behavioral impairments. Thus, our study suggests that EBP1 acts as an inhibitor of γ-secretase on amyloid precursor protein cleavage and preservation of functional EBP1 could be a therapeutic strategy for AD. Using a genome-wide association studies approach and patient brain tissue, Kim, Hwang et al. link Ebp1 to Alzheimer’s disease (AD). They show that a conditional Ebp1 knockout mouse model mimics phenotypes of sporadic AD and find that EBP1 reduces amyloid β production by inhibiting γ-secretase.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"5 3","pages":"486-503"},"PeriodicalIF":17.0,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960791","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