ArticleJournal of orthopaedic translation2025
Growth factor independence 1 ameliorates osteoarthritis by inhibiting chondrocyte ferroptosis via inactivation of MAPK signaling pathway.
Article in Journal of orthopaedic translation, 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.
- Dual-Gene Edited Extracellular Vesicles Remodel the Redox Homeostasis to Inhibit Ferroptosis in Intervertebral Disc Degeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Targeting subchondral osteoporosis in osteoarthritis: biomechanical crosstalk and the therapeutic rationale for inflammatory microenvironment remodeling.Frontiers in immunology · 2026Review
- Immuno-based profiling of knee osteoarthritis patients identifies baseline characteristics associated with positive response to autologous platelet-rich plasma injection at one-year follow-up.Frontiers in immunology · 2026Article
- Regulated Cell Death Pathways in Chondrocytes During Septic Arthritis: Current Evidence and Future Perspectives.Journal of inflammation research · 2026Review
- From scientific discovery to orthopaedic clinical innovation.Journal of orthopaedic translation · 2025Article
- Glutathione peroxidase 4 as an emerging therapeutic target in osteoarthritis: focus on ferroptosis.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
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Abstract
Background: Osteoarthritis (OA) is the most common degenerative joint disease, characterized by cartilage deterioration, which is closely associated with chondrocyte ferroptosis. The aim of this study was to investigate the role and mechanism of previously unexplored gene, growth factor independence 1 ( Methods: The expression of ferroptotic hallmarks and Gfi1 were analyzed in human and mice OA cartilages and tert-butyl hydroperoxide (TBHP)-induced primary chondrocytes. Small interfering RNA or overexpression plasmids were used to knock down or overexpress Results: The expression of Gfi1 was significantly decreased, while 4-HNE, a typical lipid peroxidation product, was significantly increased both in damaged human and DMM surgery-induced mice OA cartilages. Consistently, Gfi1 was remarkably downregulated in TBHP-induced ferroptotic chondrocytes. Moreover, Conclusion: Gfi1 is downregulated in OA and its overexpression ameliorates OA progression by inhibiting chondrocyte ferroptosis via inactivation of MAPK signaling pathway. The translational potential of this article: This study identifies Gfi1 as a novel therapeutic anti-ferroptotic target for cartilage degeneration, providing more clues for optimizing OA treatment strategies in clinical practice.
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Registered trials
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