ArticleJournal of orthopaedic surgery and research2026
From bioinformatic identification to functional validation: MMP25 as a pro-inflammatory mediator in osteoarthritis.
Article in Journal of orthopaedic surgery and 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
backgroundOsteoarthritis (OA) is a prevalent degenerative joint disorder whose pathogenesis may involve chronic inflammation. This research sought to discover new biomarkers linked to OA and to investigate their functional roles in the disease process.
methodsDifferentially expressed genes (DEGs) in OA were screened through bioinformatic analysis and subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. An in vitro model of OA was established by inducing chondrocyte degeneration using IL-1β. Expression levels of MMP25, collagen II, and aggrecan were quantified via RT-qPCR. Cell viability and apoptosis were assessed using the CCK-8 assay and the flow cytometry, respectively.
resultsBioinformatics analysis identified MMP25 upregulation in OA. Elevated MMP25 levels were observed in individuals with knee osteoarthritis and in IL-1β-exposed CHON-001 chondrocytes. Silencing MMP25 attenuated the IL-1β-induced reduction in chondrocyte viability and increase in apoptosis. Furthermore, knockdown of MMP25 enhanced anabolic activity related to extracellular matrix synthesis in IL-1β-stimulated chondrocytes.
conclusionMMP25 may serve as a potential biomarker for evaluating knee osteoarthritis and it appears to mediate IL-1β-induced chondrocyte injury and extracellular matrix degradation.
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