ReviewJournal of inflammation research2024
Ferroptosis in Osteoarthritis: Current Understanding.
Review in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The trial behind it
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Who cites it
24 citing papers in PubMed.
- Vestitol Ameliorates Ferroptosis-Associated Features and Osteoarthritis Progression Through Modulation of the GSK3B/Nrf2/GPX4 Pathway.Cell biochemistry and biophysics · 2026Article
- Signal-driven interplay between lipid peroxidation and ferroptosis orchestrates osteoarthritis degeneration.Journal of orthopaedic translation · 2026Review
- Vitexin Alleviates Osteoarthritis Progression Through Sirtuin 3-Mediated Inhibition of Chondrocyte Ferroptosis and Mitochondrial Dysfunction.Phytotherapy research : PTR · 2026Article
- Mechanism of RORα in promoting osteoarthritis through p53 deubiquitination-mediated chondrocyte ferroptosis.iScience · 2026Article
- Iron as a Key Mediator of Chronic Joint Damage: Insights from Hemophilic Arthropathy and Implications for Osteoarthritis.Medicina (Kaunas, Lithuania) · 2026Review
- A kinetic-based framework for the selection of in vitro osteoarthritis models: integrating temporal dynamics of inflammatory inducers.Molecular biology reports · 2026Review
- Elucidating the mechanism of taurine in alleviating osteoarthritis progression based on bioinformatics, machine learning algorithm, and experimental validation.Arthritis research & therapy · 2026Article
- Chronic low-dose iron exposure induces GPX4-mediated resistance to ferroptosis in a human chondrocyte cell line.Cell and tissue research · 2026Article
- Bulk and single-cell transcriptome analyses combined with molecular simulations identify ferritinophagy as a key target for resveratrol in osteoarthritis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- CircTspan3 Promotes Cartilage Development Through ANNEXIN A2-Mediated Ferroptosis and Apoptosis Inhibition and Exosome-Mediated Paracrine Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- TRIM62 promotes osteoarthritis progression by facilitating GPX4 ubiquitination and chondrocyte ferroptosis.American journal of translational research · 2026Article
- NF-κB signaling in osteoarthritis: integrating mechanical stress, innate immunity, and cartilage degeneration.Frontiers in immunology · 2026Review
- Lipid metabolic reprogramming in osteoarthritis: cartilage-centered mechanisms, whole-joint interactions, and therapeutic challenges.Frontiers in endocrinology · 2026Review
- Research progress of cuproptosis, ferroptosis, apoptosis, and autophagy in knee osteoarthritis.Frontiers in cell and developmental biology · 2026Review
- Potential crosstalk between ferroptosis and immunosenescence in osteoarthritis: evidence integration and translational insights from the osteoimmune microenvironment.Frontiers in immunology · 2026Review
- Multimodal modulation of metal-based nanomaterials in osteoarthritis immunotherapy: current landscape and future paradigms.Frontiers in immunology · 2026Review
- Lactate-driven lactylation reprograms chondrocyte fate and joint inflammation in osteoarthritis: linking metabolism with epigenetic regulation.Frontiers in cell and developmental biology · 2026Review
- The Nrf2/HO-1 signaling pathway in arthritis: from molecular mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- The emerging role of histone acetylation in rheumatic diseases: unraveling mechanisms and therapeutic prospects.Frontiers in immunology · 2026Review
- Prognostic model for osteoarthritis combining imaging and clinical biomarkers.Frontiers in medicine · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a prevalent degenerative disease in elderly people that is characterized by cartilage loss and abrasion, leading to joint pain and dysfunction. The aetiology of OA is complicated and includes abnormal mechanical stress, a mild inflammatory environment, chondrocyte senescence and apoptosis, and changes in chondrocyte metabolism. Ferroptosis is a regulated cell death modality characterized by the excessive accumulation of lipid peroxidation and mitochondrial dysfunction. The role of ferroptosis in OA pathogenesis has aroused researchers' attention in the past two years, and there is mounting evidence indicating that ferroptosis is destructive. However, the impact of ferroptosis on OA and how the regulators of ferroptosis affect OA development are unclear. Here, we reviewed the current understanding of ferroptosis in OA pathogenesis and summarized several drugs and compounds targeting ferroptosis in OA treatment. The accumulation of intracellular iron, the trigger of Fenton reaction, the excessive production of ROS, the peroxidation of PUFA-PLs, and mitochondrial and membrane damage are involved in chondrocyte ferroptosis. System X
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Registered trials
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