ArticleJournal of cellular and molecular medicine2026
Artemotil Attenuates Fibrosis-Associated Chondrocyte Remodelling in Osteoarthritis in Association With STC1-Related TGF-β/SMAD2/3 Signalling.
Article in Journal of cellular and molecular medicine, 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
Cartilage fibrosis contributes to extracellular matrix remodelling and structural deterioration during osteoarthritis (OA) progression; however, the molecular regulators involved in this process remain incompletely understood. Stanniocalcin-1 (STC1) has been implicated in tissue remodelling and fibrosis-associated signalling, but its role in chondrocyte fibrotic phenotype transition remains unclear. In this study, primary mouse chondrocytes stimulated with interleukin-1β (IL-1β), a destabilization of the medial meniscus (DMM) mouse model, and human OA cartilage samples were used to investigate the involvement of STC1 in OA-associated fibrotic remodelling. Quantitative proteomic profiling identified STC1 as a differentially regulated candidate associated with inflammatory and fibrotic responses. STC1 expression was elevated under OA-related conditions and was accompanied by increased SMAD2/3 phosphorylation. In SW1353 chondrosarcoma-derived chondrocytic cells, STC1 overexpression enhanced fibrosis-associated phenotypic changes, including increased COL1A1, ADAMTS5, and MMP-3 expression, reduced COL2A1 expression, and increased SMAD2/3 phosphorylation. Pharmacological modulation experiments further supported an association between STC1 and TGF-β/SMAD2/3 signalling activity. Artemotil attenuated fibrotic and catabolic responses in IL-1β-stimulated chondrocytes, reduced cartilage degeneration in DMM-induced OA, and was associated with reduced STC1 expression and reduced SMAD2/3 phosphorylation. Restoration of STC1 expression partially attenuated the effects of Artemotil on fibrosis-related markers and signalling alterations. These findings support a functional association between STC1, TGF-β-responsive SMAD2/3 signalling, and fibrosis-associated chondrocyte remodelling in OA and identify this signalling relationship as responsive to Artemotil intervention.
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