ArticleRMD open2026
RA-risk synovium exhibits DNA damage coupled with impaired DNA repair in fibroblasts.
Article in RMD open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Siweixizangmaoru Decoction Alleviates Rheumatoid Arthritis by Enhancing Pol β-Mediated Attenuation of DNA Damage and Suppression of cGAS/STING/NF-κB/NLRP3-Associated Pyroptosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Pre-arthritis stages of rheumatoid arthritis: from pathology to precision prevention.RMD open · 2026Article
- Preclinical Rheumatoid Arthritis: Pathogenesis, Risk Stratification, and Therapeutic Interception.Journal of clinical medicine · 2026Review
- Genotoxic stressors mimicking synovial microenvironment modulate B cell fate in RA-FLS co-culture.Frontiers in immunology · 2026Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesUnderstanding the molecular changes in the preclinical synovium is crucial for identifying factors that drive arthritis development. Persistent DNA damage in tissues is known to drive a senescent microenvironment, genomic instability and ultimately chronic inflammation. Here, we determined cellular DNA damage and repair capacity within synovial tissue from rheumatoid arthritis (RA) patients and individuals at risk of developing RA.
methodsWe investigated the presence of senescence-associated DNA damage in synovial biopsies and synovial fibroblasts obtained during different phases of RA. Histone 2A is phosphorylated (γH2AX) at the site of a double-stranded DNA break where DNA repair proteins are recruited and is therefore a proxy measurement for DNA damage. In this study, we employed immunofluorescence staining for γH2AX on synovial tissue sections and cultured synovial fibroblasts alongside quantitative PCR for a panel of DNA repair proteins.
resultsWe demonstrated the presence of DNA damage in both synovial fibroblasts and T cells during the preclinical, RA-risk phase of disease. Furthermore, cultured synovial fibroblasts from RA-risk individuals and RA patients exhibited increased DNA damage and a reduced capacity for DNA repair compared with synovial fibroblasts from control individuals. Finally, treatment with senolytic drugs partially restored the DNA damage repair capacity in RA and RA-risk synovial fibroblasts in vitro.
conclusionsOur findings reveal persistent DNA damage in the preclinical phase of RA in both synovial tissue and fibroblasts, suggesting a role in disease progression. The partial restoration of DNA repair in synovial fibroblasts by senolytic treatment highlights its potential therapeutic target for preventative therapy in RA-risk individuals.
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