ArticleNature aging2025
Recurrent somatic mutation and progerin expression in early vascular aging of chronic kidney disease.
Article in Nature aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Effects of intensive blood pressure control on cardio-kidney outcomes by KDIGO risk categories: a Post Hoc analysis of ACCORD-BP and SPRINT trials.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Article
- Single-cell analysis of the progeria arterial wall reveals progerin-induced progressive, cell type-specific dysfunction and somatic mutation accumulation.Genome medicine · 2026Article
- Reaching for the cure as progeria research comes of age at the 12th international scientific workshop.Nature aging · 2026Article
- Progerin-induced nuclear envelope remodeling is shaped by cell division and NUP153.Journal of cell science · 2026Article
- Review
- Vascular Aging.Circulation · 2026Review
- Article
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Authors and funding
24 authors.
Funding
Abstract
Early vascular aging plays a central role in chronic kidney disease (CKD), but its molecular causes remain unclear. Somatic mutations accumulate in various cells with age, yet their functional contribution to aging tissues is not well understood. Here we found progerin, the protein responsible for the premature aging disease Hutchinson-Gilford progeria syndrome, steadily recurring in vascular smooth muscle cells of patients with CKD. Notably, the most common progeria-causing mutation, LMNA c.1824C>T, was identified as a somatic mutation in CKD arteries. Clusters of proliferative progerin-expressing cells in CKD arteries and in vivo lineage-tracing in mice revealed clonal expansion capacity of mutant cells. Mosaic progerin expression contributed to genomic damage, endoplasmic reticulum stress and senescence in CKD arteries and resulted in vascular aging phenotypes in vivo. These findings suggest that certain somatic mutations may be clonally expanded in the arterial wall, contributing to the disease-related functional decline of the tissue.
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