ArticleJournal of orthopaedic surgery and research2025
RRM2 contributes to pathogenic phenotype of fibroblast-like synoviocytes by activating NF-κB signaling and inhibiting ferroptosis in rheumatoid arthritis.
Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Rheumatoid factor production is genetically and molecularly distinct from rheumatoid arthritis.The Journal of clinical investigation · 2026Article
- Downregulation of the host ribonucleotide reductase subunit M2 via the Wnt/β-catenin pathway is a novel mechanism for duck plague virus replication and a potential antiviral target.Poultry science · 2026Article
- Ferroptosis as a therapeutic nexus: traditional Chinese medicine interventions in rheumatoid arthritis.Frontiers in immunology · 2026Review
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4 authors.
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Abstract
objectiveThe development and pathogenesis of rheumatoid arthritis (RA) are associated with ferroptosis. This study aims to investigate the regulatory role of ribonucleotide reductase subunit M2 (RRM2) in ferroptosis and the pathogenic phenotype of fibroblast-like synoviocytes (FLSs) in RA.
methodsTranscriptomic datasets associated with rheumatoid arthritis were analyzed to identify differentially expressed genes (DEGs), which were then intersected with known ferroptosis-related genes using a Venn diagram to determine overlapping candidates. The receiver operating characteristic (ROC) curve was utilized to evaluate the diagnostic value of key genes. The expression of RRM2 was silenced using short hairpin RNA transfection. Cell viability, motility, and invasive capacity were evaluated through the CCK-8 assay, scratch assay, Transwell, and ELISA assay, respectively. Inflammatory cytokines and ferroptosis-associated indicators were quantified using ELISA and specific biochemical detection kits. Additionally, the transcriptional and protein levels of genes linked to FLS function were analyzed.
resultsRRM2 was upregulated in tumor necrosis factor-alpha (TNF-α)-induced MH7A cells. Knockdown of RRM2 significantly inhibited TNF-α-induced cell proliferation, migration, invasiveness, and the release of pro-inflammatory cytokines in MH7A cells. Additionally, RRM2 knockdown induced ferroptosis, as evidenced by increased reactive oxygen species (ROS), ferrous iron (Fe
conclusionRRM2 inhibits ferroptosis and enhances the pathogenic behavior of RA FLSs through activation of the NF-κB pathway, highlighting its pivotal contribution to RA development.
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