ArticleNature aging2025
Single-cell analysis of the somatic mutational landscape in human chondrocytes during aging and in osteoarthritis.
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.
What it found
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Who cites it
7 citing papers in PubMed.
- Advancing aging biomarkers and intervention discovery at the TimePie Longevity Forum.Nature aging · 2026Article
- Article
- Motif-Centered Analyses Reveal Universal and Tissue-Specific Mutagenic Mechanisms Operating in the Human Body.bioRxiv : the preprint server for biology · 2026Article
- Comparative whole-genome analyses of articular chondrocytes and skin fibroblasts reveal distinct genome instability landscapes in mesenchymal cell types.PLoS genetics · 2026Article
- Comparative whole-genome analyses of articular chondrocytes and skin fibroblasts reveal distinct genome instability landscapes in mesenchymal cell types.bioRxiv : the preprint server for biology · 2026Article
- Mechano-immune interactions in musculoskeletal aging: Mechanisms and translational perspectives.Theranostics · 2026Review
- Biomarkers of aging as it relates osteoarthritis: we can't improve what we can't measure.Connective tissue research · 2025Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Somatic mutation is now recognized as a cause of multiple human diseases other than cancer. Osteoarthritis (OA), a highly prevalent age-related disease, has been associated with increased chromosomal abnormalities in articular cartilage. Here we characterize the somatic mutational landscape of chondrocytes during normal aging and in affected cartilage of patients with OA. We used single-cell whole-genome sequencing to analyze single-nucleotide variants (SNVs) and small insertions and deletions (InDels) in 100 chondrocytes isolated from the cartilage of hip femoral heads of 17 research participants aged 26-90 years, including 9 patients with OA and 8 non-OA donors. Both SNVs and InDels accumulate with age in chondrocytes with a clock-like mutational signature. Surprisingly, the age-related accumulation rate in OA chondrocytes is lower than that in non-OA control chondrocytes. Differences in mutational signatures and Gene Ontology term enrichment were found between OA and non-OA control samples. In this study, to understand the role of somatic mutation in the pathogenesis of OA, we characterized somatic SNV and InDel mutations. With further progress in analytical approaches, structural variations in the chondrocyte genome are also expected to provide valuable information.
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