ArticleOpen life sciences2025
SIK1 inhibits IL-1β-stimulated cartilage apoptosis and inflammation
Article in Open life sciences, 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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3 authors.
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Abstract
Osteoarthritis (OA) is a chronic degenerative joint disease that affects 70-90% of individuals over the age of 75 and over 100 million people globally. Current treatments primarily offer symptomatic relief and do not effectively halt disease progression, highlighting the need for improved therapeutic strategies. Salt-inducible kinase 1 (SIK1) plays a role in regulating key physiological processes, including gluconeogenesis, glycolysis, and bone metabolism. Despite these insights, the specific role and underlying mechanisms of SIK1 in OA pathogenesis remain inadequately understood. This study aims to elucidate the function of SIK1 in OA cells. We observed that SIK1 was downregulated in a cell model of OA. The overexpression of SIK1 was found to inhibit IL-1β-induced chondrocyte apoptosis and inflammation. Additionally, SIK1 overexpression enhanced the activation of the CRTC2/CREB1 axis, suggesting a protective role for SIK1 in cartilage cells. In summary, SIK1 exerts a protective effect against IL-1β-induced cartilage apoptosis and inflammation
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