Nature aging最新文献

A consensus roadmap from the SENESCENCE2030 network towards precision senescence medicine. SENESCENCE2030网络面向精准衰老医学的共识路线图。

IF 25

Nature aging Pub Date : 2026-09-03 DOI: 10.1038/s43587-026-01222-y

Aniello Cerrato, Antonella Farsetti, Laura Bordoni, Raquel Rua Martins, Iker Bengoetxea de Tena, Ivana Vrhovac Madunic, Marziyya Mammadova, Stefano Raviola, Mohamad Rima, Minenur Ozturk, Rosa Spinelli, Nicoleta Moisoi, Francesco Nicoli, Luca Pangrazzi, An Wouters, Ashraf Albrakati, Mahmoud Abdellatif, Lorna W Harries, Giuseppe Martini, Yannis Missirlis, Brunella Mongiardi, Sonia de Pascual-Teresa, Daniel Moreno-Blas, Ayse Cakir Gungor, Diana Cunha-Reis, Cleo L Bishop, Johannes Grillari, Pasquale Maffia, Marco Demaria

引用次数: 0

GLP-1 receptor agonism extends median lifespan in mice. GLP-1受体激动作用延长小鼠的中位寿命。

IF 25

Nature aging Pub Date : 2026-09-03 DOI: 10.1038/s43587-026-01224-w

Anna Kriebs

引用次数: 0

Reframing the epidemiological transition as increasing returns to tackling aging-related diseases. 重新定义流行病学转变，增加应对与老龄化有关疾病的回报。

IF 25

Nature aging Pub Date : 2026-09-02 DOI: 10.1038/s43587-026-01210-2

Julian Ashwin, David E Bloom, Naomi Lee, Peter Piot, Andrew J Scott

引用次数: 0

Multimorbidity patterns influence mobility disability prevention in frail older adults from the SPRINTT trial. SPRINTT试验中多病模式影响体弱老年人的行动能力残疾预防。

IF 25

Nature aging Pub Date : 2026-08-31 DOI: 10.1038/s43587-026-01188-x

Davide Liborio Vetrano, Caterina Gregorio, Federico Triolo, Luca Soraci, Antonio Cherubini, Matteo Tosato, Stephan von Haehling, Emanuele Marzetti, Francesco Landi, Riccardo Calvani

{"title":"Multimorbidity patterns influence mobility disability prevention in frail older adults from the SPRINTT trial.","authors":"Davide Liborio Vetrano, Caterina Gregorio, Federico Triolo, Luca Soraci, Antonio Cherubini, Matteo Tosato, Stephan von Haehling, Emanuele Marzetti, Francesco Landi, Riccardo Calvani","doi":"10.1038/s43587-026-01188-x","DOIUrl":"https://doi.org/10.1038/s43587-026-01188-x","url":null,"abstract":"Preserving independence in older adults is a public health priority. Lifestyle interventions can prevent physical disability, but whether their efficacy is influenced by multimorbidity profiles is unclear. In this post hoc analysis of the SPRINTT randomized trial ( NCT02582138 ), we investigated whether the efficacy of a multicomponent intervention (physical activity with technological support and nutritional counseling) differed across multimorbidity patterns. We included 1,199 community-dwelling adults aged ≥70 years with frailty, sarcopenia and two or more chronic conditions. Latent class analysis identified four multimorbidity patterns: unspecific (55%), psychiatric (24%), cardiometabolic (13%) and respiratory (7%). The intervention reduced the overall risk of mobility disability or death (hazard ratio (HR) 0.78, 95% confidence interval (CI) 0.66-0.92). In subgroup analyses, a significant benefit was observed in participants with a psychiatric multimorbidity pattern (HR 0.65, 95% CI 0.47-0.92). Bayesian partial pooling analyses also supported a beneficial effect in the unspecific pattern (HR 0.80, 95% credible interval 0.69-0.93), while estimates for the cardiometabolic and respiratory patterns were imprecise and not statistically significant. The intervention increased the event-free probability at 24 and 36 months and extended the time free from mobility disability or death by 2.09 months overall. Gains were 3.09 months in the psychiatric pattern and 1.99 months in the unspecific pattern, with no meaningful differences observed in the cardiometabolic and respiratory patterns. These findings suggest that the composition of multimorbidity may influence responsiveness to lifestyle interventions and that stratification based on disease patterns could improve the targeting and effectiveness of preventive strategies in older adults.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":25.0,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148868535","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

Mapping structural aging across human tissues reveals tissue-specific trajectories and coordinated deterioration. 绘制人体组织结构老化图揭示了组织特异性轨迹和协调退化。

IF 25

Nature aging Pub Date : 2026-08-31 DOI: 10.1038/s43587-026-01200-4

Anamika Yadav, Kyle Alvarez, Anna Chechenina, Kevin Y Yip, Eytan Ruppin, Alexandre Colas, Jacqueline C Yano Maher, Veronica Gomez-Lobo, Caroline Kumsta, Sanju Sinha

{"title":"Mapping structural aging across human tissues reveals tissue-specific trajectories and coordinated deterioration.","authors":"Anamika Yadav, Kyle Alvarez, Anna Chechenina, Kevin Y Yip, Eytan Ruppin, Alexandre Colas, Jacqueline C Yano Maher, Veronica Gomez-Lobo, Caroline Kumsta, Sanju Sinha","doi":"10.1038/s43587-026-01200-4","DOIUrl":"https://doi.org/10.1038/s43587-026-01200-4","url":null,"abstract":"Organ structure, including the organization of cells, vasculature and extracellular matrix, underpins its function, yet how structure changes with age remains mostly unknown. Here we developed PathStAR, a framework that quantifies tissue structural aging from routine histopathology images, without being trained to predict chronological age. Applying PathStAR to 25,306 post-mortem biopsies from 40 tissues in 970 donors aged 21-70 years revealed that organ structural aging progresses via distinct, nonlinear temporal trajectories: vascular tissue structural aging accelerates early, uterus and vagina structural aging accelerates late (around menopause) and certain tissues including digestive and male reproductive organs show biphasic accelerations. We show that accelerations of structural aging are characterized across organs by increased inflammation alongside reduced energy production, repair and quality control. Cross-organ analysis reveals coordinated deterioration within individuals, including digestive and male reproductive tissues, linked by sex hormones. Together, our analysis provides a systematic map of structural aging across the human body.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":25.0,"publicationDate":"2026-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148868544","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

Leaky oocytes propagate cGAS-STING signaling. 漏卵细胞传播cGAS-STING信号。

IF 25

Nature aging Pub Date : 2026-08-28 DOI: 10.1038/s43587-026-01153-8

Subhasri Biswas, Michael B Stout

引用次数: 0

Mitochondrial DNA leakage in oocytes activates cGAS-STING signaling to drive ovarian aging. 卵母细胞线粒体DNA渗漏激活cGAS-STING信号，促进卵巢衰老。

IF 25

Nature aging Pub Date : 2026-08-28 DOI: 10.1038/s43587-026-01195-y

Min Lei, Zhenye Zhu, Huihui Xie, Chenlu Wei, Jiajia Zhu, Keer Wang, Kexin Zhang, Yongxing Yu, Linli Yang, Xiangyang Zhang, Ning Song, Diyi Xie, Ruizhi Guo, Yanqing Zhao, Aaron J W Hsueh, Yingpu Sun, Qingling Yang

{"title":"Mitochondrial DNA leakage in oocytes activates cGAS-STING signaling to drive ovarian aging.","authors":"Min Lei, Zhenye Zhu, Huihui Xie, Chenlu Wei, Jiajia Zhu, Keer Wang, Kexin Zhang, Yongxing Yu, Linli Yang, Xiangyang Zhang, Ning Song, Diyi Xie, Ruizhi Guo, Yanqing Zhao, Aaron J W Hsueh, Yingpu Sun, Qingling Yang","doi":"10.1038/s43587-026-01195-y","DOIUrl":"https://doi.org/10.1038/s43587-026-01195-y","url":null,"abstract":"Ovarian aging precedes decline in many organs, but its mechanisms remain unclear. Here we show that aging oocytes accumulate cytoplasmic mitochondrial DNA (mtDNA) through increased mtDNA leakage, activating the cyclic GMP-AMP synthase (cGAS) pathway to produce cGAMP and trigger stimulator of interferon genes (STING) signaling. Notably, oocyte-derived cGAMP can pass through gap junctions to surrounding granulosa cells (GCs), activating STING signaling in GCs as well. To model age-associated mitochondrial dysfunction, we generated oocyte-specific Tfam-knockout mice, which recapitulated mtDNA leakage, STING pathway activation in both oocytes and GCs, inflammation and accelerated ovarian dysfunction. We also used Opa1 knockdown and Pink1 deletion oocytes as complementary mitochondrial stress models and observed mtDNA leakage and cGAS-STING activation in both settings. Notably, oocyte-specific Cgas deletion in Tfam mutants or pharmacological STING inhibition with H-151 ameliorated ovarian dysfunction. These findings establish oocyte mtDNA leakage as a causal driver of ovarian aging and nominate cGAS-STING signaling as a therapeutic target.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":25.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148852316","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

Closing the gap in Alzheimer's disease research through the Sex | Gender in Neurodegeneration Consortium. 通过性|神经变性性别联盟缩小阿尔茨海默病研究的差距。

IF 25

Nature aging Pub Date : 2026-08-28 DOI: 10.1038/s43587-026-01214-y

Caitlin P McHugh, Rachel F Buckley, Matthew H S Clement, Timothy J Hohman, Miia Kivipelto, Judy Pa, Shireen Sindi, Niranjan Bose

引用次数: 0

Contracting myografts mimic exercise response. 收缩肌移植物模拟运动反应。

IF 25

Nature aging Pub Date : 2026-08-26 DOI: 10.1038/s43587-026-01191-2

James P White

引用次数: 0

Cytotoxic CD4⁺ T cells induce age-associated myelopoiesis through CCL5-CCR5 signaling. 细胞毒性CD4+ T细胞通过CCL5-CCR5信号传导诱导年龄相关性骨髓生成。

IF 25

Nature aging Pub Date : 2026-08-26 DOI: 10.1038/s43587-026-01209-9

Enrique Gabandé-Rodríguez, Gonzalo Soto-Heredero, Elisa Carrasco, Carlos Anerillas, José Ignacio Escrig-Larena, Jorge Martínez-Cano, Sandra Delgado-Pulido, Isaac Francos-Quijorna, Gabriela Desdín-Micó, Tatiana Smirnova, Manuel M Gómez de Las Heras, Álvaro Fernández-Almeida, Alice Leandri, Andrea Cugurra, Eva María Blanco, Elia Winand-Osete, Pablo Ramírez-Ruiz de Erenchun, Virginia Zorita, Camilla Bean, Valentin Basset, Françoise Solly, Amanda Garrido, Rafael de Cabo, Santos Mañes, Manolis Pasparakis, Matteo Iannacone, César Cobaleda, Olaia Naveiras, Myriam Gorospe, María Mittelbrunn

{"title":"Cytotoxic CD4+ T cells induce age-associated myelopoiesis through CCL5-CCR5 signaling.","authors":"Enrique Gabandé-Rodríguez, Gonzalo Soto-Heredero, Elisa Carrasco, Carlos Anerillas, José Ignacio Escrig-Larena, Jorge Martínez-Cano, Sandra Delgado-Pulido, Isaac Francos-Quijorna, Gabriela Desdín-Micó, Tatiana Smirnova, Manuel M Gómez de Las Heras, Álvaro Fernández-Almeida, Alice Leandri, Andrea Cugurra, Eva María Blanco, Elia Winand-Osete, Pablo Ramírez-Ruiz de Erenchun, Virginia Zorita, Camilla Bean, Valentin Basset, Françoise Solly, Amanda Garrido, Rafael de Cabo, Santos Mañes, Manolis Pasparakis, Matteo Iannacone, César Cobaleda, Olaia Naveiras, Myriam Gorospe, María Mittelbrunn","doi":"10.1038/s43587-026-01209-9","DOIUrl":"https://doi.org/10.1038/s43587-026-01209-9","url":null,"abstract":"Age-associated hematopoietic skewing results in an increase in the neutrophil-to-lymphocyte ratio, which serves as a strong predictor of all-cause mortality in older adults, although its causes are incompletely understood. Here we show that cytotoxic CD4+ T lymphocytes accumulate in the bone marrow of mice during aging and induce myelopoiesis, increasing the neutrophil-to-lymphocyte ratio. T cell receptor-dependent induction of mitochondrial stress and activation of STING upregulates the chemokine CCL5 in CD4+ T lymphocytes. During aging, hematopoietic stem cells and downstream myeloid progenitors upregulate CCR5, the primary receptor for CCL5. Genetic ablation of Ccr5 in hematopoietic progenitors mitigates T cell-induced myeloid skewing and neutrophil expansion. Pharmacological blockade of CCR5 using the Food and Drug Administration-approved drug maraviroc normalizes myelopoiesis, reduces circulating and tissue-infiltrating neutrophils, and improves multiple aging-related biomarkers and functional outcomes in aged mice. Together, these findings demonstrate a T cell-bone marrow axis that exacerbates age-associated decline and highlight CCR5 inhibition as a potential geroprotective strategy.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":25.0,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148835704","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