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27 parsed articles
Last update: 2026-09-22
2026-09-21
Shuai Ma, Jing Qu
Senescence has traditionally been studied largely on the basis of changes in gene expression, but senescent cells also undergo profound biochemical remodeling. Zhang and colleagues introduce RamanOmics, a multimodal approach that links Raman-based chemical imaging with spatial transcriptomics to reveal the hidden biochemical landscape of cellular senescence.
DOI: 10.1038/s43587-026-01230-y2026-09-21
Ke Zhang, Xingjian Chen, Francesco Monticolo, Salvatore Sorrentino, Haochun Huang, Claire Callahan, Yueqing Qiao, Judy Zhou, Sonia Brodowska, Styliani Sapantzi, Jianhuan Qi, Yinghan Wu, Thai Nam Son Dang, Yanwan Cao, Sumin Kang, Francesca Viggiani, Chia-Kang Ho, Yanxin Xu, Koseki J. Kobayashi-Kirschvink, Thang Mung, Hemali Phatnani, Zhixun Dou, Jeon Woong Kang, Peter T. C. So, Jian Shu
Zhang, Chen, Monticolo, Sorrentino and colleagues pair label-free Raman imaging with spatial and single-cell transcriptomics to probe biochemical signatures of senescence in aging and repair, identifying a lipid-linked Raman signature of p21+ cells.
DOI: 10.1038/s43587-026-01219-72026-09-18
Aging is associated with myeloid-biased hematopoiesis, which leads to the establishment of a pro-inflammatory microenvironment. We discovered that cytotoxic CD4+ T cells foster this process via the CCL5–CCR5 axis and found that the clinically approved CCR5 antagonist maraviroc can rebalance immunity in aged mice.
DOI: 10.1038/s43587-026-01241-92026-09-16
Arturo D’Angelo, Daniel Franco-Barranco, Marco Musy, Juan Manuel Duran, James Sharpe, Nicholas Stroustrup, Ignacio Arganda-Carreras, Elvan Böke
DOI: 10.1038/s43587-026-01244-62026-09-14
Brendan Miller, Eduardo Vieira de Souza, Calvin Lau, Joan M. Vaughan, Victor J. Pai, Servando Giraldez, Andréa Rocha, Jolene K. Diedrich, Clodagh C. O’Shea, David A. Bennett, Alan Saghatelian
A new atlas identifies 1,067 unannotated microproteins in the human frontal cortex with strong spectral grades. A subset is differentially expressed in Alzheimer’s disease independently of their canonical genes, including an MKKS-derived microprotein required for normal microglial mitochondrial respiration.
DOI: 10.1038/s43587-026-01207-x2026-09-14
Microproteins, small proteins of 100–150 amino acids, are largely absent from reference proteomes and have been overlooked in brain and aging research. An atlas of the aged human brain catalogs over 1,000 high-confidence microproteins, including one encoded by the MKKS gene that is reduced in Alzheimer’s disease and regulates energy production in microglia.
DOI: 10.1038/s43587-026-01215-x2026-09-11
Prabesh Bhattarai, Elanur Yilmaz, Elif Öykü Cakir, Huseyin Tayran, Imdadul Haq, Dylan Murphy, Jonah Nadelmann Keller, Quentin Le Grand, Jacqueline O. Eschbach, Hilal Celikkaya, Mehmet I. Cosacak, Hande Yüceer Korkmaz, Annie J. Lee, Verena Haage, Yiyi Ma, Xue Wang, Nastasia Nelson, Weilin Lin, Yixin Zhang, Bengisu Turgutalp, Sherida M. de Leeuw, Ronak Patel, Dörthe Jülich, Özkan İş, Scott A. Holley, Philip L. De Jager, Uwe Freudenberg, Carsten Werner, Peter St George-Hyslop, Nilüfer Ertekin-Taner, Stéphanie Debette, Fanny M. Elahi, Elizabeth S. Fisher, Hemali Phatnani, Andrew F. Teich, Kate Tubbesing, Taylor Bertucci, Sally Temple, Tal Nuriel, Badri N. Vardarajan, Richard Mayeux, Caghan Kizil
Bhattarai, Yilmaz and colleagues identify astrocyte-derived fibronectin as a key driver of blood–brain barrier dysfunction in Alzheimer’s disease, linking APOE ε4 and amyloid pathology to vascular damage and highlighting FN1 as a potential therapeutic target.
DOI: 10.1038/s43587-026-01204-02026-09-11
Orsolya Symmons
DOI: 10.1038/s43587-026-01193-02026-09-07
Joseph L. Dieleman
Ashwin and colleagues propose a statistical framing of the epidemiological transition that categorizes global diseases into four life-stages, identifying aging-related diseases as the dominant category. As aging-related diseases tend to cluster and span many years, health systems must pivot from treating disease to preserving health through investments in all life stages.
DOI: 10.1038/s43587-026-01218-82026-09-07
Hongkai Zhao, Qianzhao Ji, Zeming Wu, Si Wang, Jie Ren, Kaowen Yan, Zehua Wang, Jianli Hu, Qun Chu, Huifang Hu, Yusheng Cai, Qiaoran Wang, Daoyuan Huang, Zhejun Ji, Jingyi Li, Juan Carlos Izpisua Belmonte, Moshi Song, Weiqi Zhang, Jing Qu, Guang-Hui Liu
DOI: 10.1038/s43587-026-01235-72026-07-24
Mariah F. Calubag
Nature Aging, Published online: 24 July 2026; doi:10.1038/s43587-026-01169-0 Calubag et al. report that reduced dietary intake of the branched-chain amino acid valine is sufficient to improve healthspan in both male and female mice, as well as to extend lifespan in male mice.]]>
DOI: 10.1038/s43587-026-01169-02026-07-17
Boshi Wang
Nature Aging, Published online: 17 July 2026; doi:10.1038/s43587-026-01168-1 Wang et al. report that the cell cycle regulators CDK4/6 also regulate the inflammatory phenotype of senescent cells, via modulation of retinoic acid signaling and NF-κB. Pharmacologically targeting this pathway reduces inflammation and improves physical function in models of chemotherapy-induced toxicity and aging.]]>
DOI: 10.1038/s43587-026-01168-12026-07-13
Nature Aging, Published online: 13 July 2026; doi:10.1038/s43587-026-01167-2 Single-cell spatial mapping and orthogonal approaches reveal a senescent and disease-associated microglial state that accumulates in the white matter of the aged mouse brain and is suppressed by senotherapeutic interventions.]]>
DOI: 10.1038/s43587-026-01167-22026-07-02
Meng Wu
Nature Aging, Published online: 02 July 2026; doi:10.1038/s43587-026-01159-2 The ovarian stroma becomes increasingly stiff with age, impairing ovarian function. The mechanisms that underlie this process are only partly understood. Here, the authors show that IL-11, which is elevated in aging ovaries of mice, rats and humans, activates fibroblasts to secrete extracellular matrix, increasing ovarian stiffness. Targeting IL-11 mitigates ovarian aging.]]>
DOI: 10.1038/s43587-026-01159-22026-06-24
Mahmoud Abdellatif
Nature Aging, Published online: 24 June 2026; doi:10.1038/s43587-026-01158-3 Abdellatif, Kim and Kroemer propose a pragmatic approach for the clinical evaluation of geroprotective interventions without compromising clinical priorities, aiming to improve geromedicine trial feasibility and facilitate regulatory approval.]]>
DOI: 10.1038/s43587-026-01158-32026-06-24
Raúl F. Pérez
Nature Aging, Published online: 24 June 2026; doi:10.1038/s43587-026-01152-9 Epigenetic drift leads to gradual alterations of the epigenome that have been harnessed (particularly at the DNA-methylation level) to build epigenetic clocks. However, the functional significance of the signals these clocks capture remains unclear. We discuss the evolution of the concept of epigenetic drift and examine how epigenetic clocks have emerged as quantitative readouts of this phenomenon.]]>
DOI: 10.1038/s43587-026-01152-92026-06-22
James G. Peyer
Nature Aging, Published online: 22 June 2026; doi:10.1038/s43587-026-01165-4 Are GLP-1 receptor agonists gerotherapeutics or just treatments for obesity?]]>
DOI: 10.1038/s43587-026-01165-42026-06-18
Maria Eriksson
Nature Aging, Published online: 18 June 2026; doi:10.1038/s43587-026-01142-x In October 2025, The Progeria Research Foundation convened its 12th International Scientific Workshop to review recent scientific advances in Hutchinson–Gilford progeria syndrome (HGPS) and other progeroid diseases and to identify priorities for therapeutic development. This Meeting Report highlights key considerations from the workshop for advancing progeria research, and its relevance to cardiovascular disease and aging.]]>
DOI: 10.1038/s43587-026-01142-x2026-06-17
Jing Hou
Nature Aging, Published online: 17 June 2026; doi:10.1038/s43587-026-01130-1 Hou, Chen and colleagues profile the effects of dasatinib and quercetin senolytic treatment on aged male mice across tissues, using bulk, single-cell and single-nucleus transcriptomics, reporting effects on immunity, fibrosis and metabolism, with early and prolonged intervention showing stronger efficacy.]]>
DOI: 10.1038/s43587-026-01130-12026-06-12
Nature Aging, Published online: 12 June 2026; doi:10.1038/s43587-026-01141-y We developed a mathematical framework that maps survival data onto cellular damage dynamics, which revealed two distinct aging regimes across species. This unified model explains why and how aging patterns diverge and provides a quantitative basis for comparing aging in model organisms and extrapolating findings to human biology.]]>
DOI: 10.1038/s43587-026-01141-y2026-06-05
Timothy Y. Chang
Nature Aging, Published online: 05 June 2026; doi:10.1038/s43587-026-01145-8 A new study conducted by Iiams and colleagues reveals that lifelong time-restricted feeding of a standard diet to non-obesogenic mice can extend healthspan, with sex-specific effects on aging-associated pathologies and lifespan.]]>
DOI: 10.1038/s43587-026-01145-82026-06-02
Zane Koch
Nature Aging, Published online: 02 June 2026; doi:10.1038/s43587-026-01132-z The DREAM complex is a transcriptional repressor of DNA repair. Koch et al. infer DREAM activity via expression of its repressed targets and use DREAM knockout mice to link DREAM activity to somatic mutation burden, age-related disease and lifespan.]]>
DOI: 10.1038/s43587-026-01132-z2026-05-28
Laura Ward
Nature Aging, Published online: 28 May 2026; doi:10.1038/s43587-026-01133-y On 4–6 September 2025, the Gulbenkian Institute for Molecular Medicine (GIMM) hosted its inaugural GIMM Festival in Lisbon, Portugal. The three-day meeting on ‘Aging and Longevity’ brought together researchers, clinicians, artists and civil society to reflect collectively on which questions should shape the future of aging research and its societal effects. This report summarizes the scientific sessions and structured discussions, and highlights the ‘questions of the future’ that emerged as a shared roadmap for the field.]]>
DOI: 10.1038/s43587-026-01133-y2026-05-20
Arpit Sharma
Nature Aging, Published online: 20 May 2026; doi:10.1038/s43587-026-01122-1 Sharma and colleagues show that, in Caenorhabditis elegans, age-associated decline in peroxisomal function causally impairs lipid mobilization, resulting in lipid droplet accumulation, metabolic inflexibility and secondary mitochondrial dysfunction. Restoring peroxisomal activity reinstates metabolic resilience during aging.]]>
DOI: 10.1038/s43587-026-01122-12026-05-20
Andrew Zalesky
Nature Aging, Published online: 20 May 2026; doi:10.1038/s43587-026-01113-2 Zalesky and colleagues discuss the evolution of aging clocks into organ-specific aging readouts that harness omics and imaging data. They review the insights that this additional resolution provides on differential aging across organs within interconnected systems, as well as the methods, priorities and future directions.]]>
DOI: 10.1038/s43587-026-01113-22026-03-31
Shouxuan Zhu, Sunyang Ying, Donghong Cai, Ya Ren, Luoxi Wang, Zhi Qi, Vera Gorbunova, Jing-Dong J. Han
Nature Aging, Published online: 31 March 2026; doi:10.1038/s43587-026-01100-7 To dissect lncRNA functions in aging, here the authors perform a CRISPRi-based single-nucleus multiomics screen systematically perturbing 32 aging- and senescence-associated lncRNAs and measuring matched changes in gene expression and chromatin accessibility. They pinpoint a role for HOTAIRM1 linked to DNA repair-related gene control and show that replenishing HOTAIRM1 in mouse lungs reduces fibrosis.
2026-03-31
Pulkit Gupta, Eric Lee, Neus Masqué Soler, Ellen Schrader, Xiao Qian Wang, Shimrit Mayer, Cristina Flores, Sean Beatty, Andrew Roth, Samuel Aparicio, H. Raza Ali
Nature Aging, Published online: 31 March 2026; doi:10.1038/s43587-026-01104-3 The dynamics of breast tissue aging are characterized by imaging mass cytometry of over 500 reduction mammoplasties, revealing nonlinear loss of cellularity and a compositional shift favoring inflammation.