ReviewFrontiers in cell and developmental biology2025
Glutathione peroxidase 4 as an emerging therapeutic target in osteoarthritis: focus on ferroptosis.
Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Do Oxidative Stress-Modified Exosomes Contribute to Infertility in Endometriosis?International journal of molecular sciences · 2026Review
- Iron as a Key Mediator of Chronic Joint Damage: Insights from Hemophilic Arthropathy and Implications for Osteoarthritis.Medicina (Kaunas, Lithuania) · 2026Review
- Chronic low-dose iron exposure induces GPX4-mediated resistance to ferroptosis in a human chondrocyte cell line.Cell and tissue research · 2026Article
- Research progress of cuproptosis, ferroptosis, apoptosis, and autophagy in knee osteoarthritis.Frontiers in cell and developmental biology · 2026Review
- Integrated untargeted and targeted metabolomics combined with experimental validation reveal glutathione-related oxidative stress in pediatric IgA vasculitis nephritis.Frontiers in pharmacology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a degenerative joint disease characterized by articular cartilage degradation, extracellular matrix breakdown, low-grade chronic inflammation, and pain. Its etiology is complex and treatment options are limited. In recent years, ferroptosis, a regulated form of cell death driven by iron-dependent lipid peroxidation, has gained significant attention in OA pathogenesis. Glutathione peroxidase 4(GPX4), serves as the central enzyme that halts lipid peroxidation and inhibits ferroptosis. Its expression and activity are altered in OA cartilage under pathological conditions, suggesting a crucial role for GPX4 in OA pathogenesis and treatment. This review summarizes the molecular characteristics and antioxidant functions of GPX4, evaluates experimental evidence linking GPX4 and ferroptosis in OA, outlines upstream and downstream molecular mechanisms regulating GPX4, and summarizes therapeutic strategies targeting GPX4, including pharmacological, gene, and combination therapies. It also discusses current research challenges and future directions. Finally, key pathways and strategic recommendations for translating GPX4 and ferroptosis research into clinical OA treatments are proposed.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.