ArticleArthritis research & therapy2025
SGK1 triggers cartilage degradation in TMJOA via FoxO1/autophagy.
Article in Arthritis research & therapy, 2025. 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
backgroundTemporomandibular joint osteoarthritis (TMJOA) is a prevalent inflammatory disease with unclear pathogenesis. Serum and glucocorticoid-inducible kinase 1 (SGK1) has been implicated in osteoarthritis-related cartilage degeneration. This study investigated the role of SGK1 in a mouse model of TMJOA and explored its mechanism, focusing on SGK1's regulation of Forkhead box O1 (FoxO1) and its subsequent effects on autophagy and extracellular matrix degradation in mouse condylar chondrocytes (MCCs).
methodsA TMJOA model was established using unilateral anterior crossbite (UAC), and an SGK1 knockdown model was generated via intra-articular injection of AAV virus.
resultsSGK1 expression was significantly upregulated in condylar cartilage of UAC-induced TMJOA mice. SGK1 knockdown alleviated cartilage matrix degradation and increased the expression of anabolic marker. In MCCs, SGK1 directly bound to FoxO1, promoting its phosphorylation and nuclear export, thereby inhibiting autophagy. Inhibiting SGK1 enhanced autophagy, as evidenced by increased Beclin-1, elevated LC3-II/LC3-I ratio, and decreased P62, which consequently attenuated IL-1β-induced extracellular matrix catabolism. These effects were reversed by autophagy inhibitor chloroquine and FoxO1 inhibitor AS1842856.
conclusionsThis study is the first to propose the regulatory role of SGK1 in TMJOA, providing new insights for future therapeutic research.
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