ArticleAmerican journal of translational research2026
TRIM62 promotes osteoarthritis progression by facilitating GPX4 ubiquitination and chondrocyte ferroptosis.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesThis study investigates the role of Tripartite motif containing 62 (TRIM62) in osteoarthritis (OA) progression, focusing on its regulation of Glutathione Peroxidase 4 (GPX4) ubiquitination and chondrocyte ferroptosis.
methodsAn OA rat model was established via anterior cruciate ligament transection (ACLT) and then primary chondrocytes were stimulated with interleukin-1β (IL-1β) in vitro. TRIM62 expression was manipulated using short hairpin RNA (shRNA) or overexpression plasmids. Ferroptosis was assessed by measuring GPX4, solute carrier family 7 member 11 (SLC7A11), glutathione (GSH), reactive oxygen species (ROS), ferrous iron (Fe
resultsRIM62 expression was significantly increased in osteoarthritic cartilage and in chondrocytes treated with IL-1β. TRIM62 knockdown restored GPX4 and collagen type II (COL II) expression, reduced disintegrin and metalloproteinase with thrombospondin motifs 5 (ADAMTS5) levels, suppressed ferroptosis, and alleviated cartilage damage
conclusionsTRIM62 facilitates OA progression by inducing GPX4 ubiquitination and degradation, thereby promoting chondrocyte ferroptosis. The TRIM62-GPX4-ferroptosis axis represents a promising therapeutic target for OA.
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