ArticleArchives of rheumatology2025
Methylation of PRDX3 Expression Alleviate Ferroptosis and Oxidative Stress in Patients with Osteoarthritis Cartilage Injury.
Article in Archives of rheumatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Immunometabolic reprogramming in rheumatoid arthritis: the epitranscriptomic role of N6-methyladenosine in innate and adaptive immunity.Frontiers in immunology · 2026Review
- A homozygous PRDX3 pathogenic variant in a paediatric case of spinocerebellar ataxia type 32.Neurogenetics · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/Aims: Osteoarthritis typically features cartilage degeneration, synovial fibrosis, and bone remodeling. While clinical Western medicine therapies can restore joint functions, long-term use may exacerbate cartilage damage. This study was designed to investigate the impact of peroxiredoxin 3 (PRDX3) on ferroptosis and oxidative stress in osteoarthritis cartilage injury and its potential mechanism. Materials and Methods: In the osteoarthritis model, the expression of PRDX3 was downregulated. Single-cell analysis revealed that the PRDX3 gene was expressed in bone cells of osteoarthritis patients. Results: Sh-PRDX3 promoted osteoarthritis cartilage injury in the mouse model via the induction of oxidative stress. PRDX3 suppressed reactive oxygen species accumulation and mitochondria-dependent ferroptosis in the in vitro model or mice model of osteoarthritis. PRDX3 induced SIRT3 to reduce SIRT3 ubiquitin. Moreover, METTL3-mediated m6A modification decreases PRDX3 mRNA stability by YTHDF1 in the osteoarthritis cartilage injury model. Conclusion: These findings indicate that METTL3-mediated m6A modification decreases PRDX3 mRNA stability to relieve ferroptosis and oxidative stress in the model of osteoarthritis cartilage injury in a YTHDF1-dependent manner. Targeting METTL3 is thus a potentially effective therapeutic strategy for patients with osteoarthritis cartilage injury.
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Registered trials
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