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Background <p>Osteoarthritis (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.</p> Methods <p>Differentially 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.</p> Results <p>Bioinformatics 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.</p> Conclusion <p>MMP25 may serve as a potential biomarker for evaluating knee osteoarthritis and it appears to mediate IL-1β-induced chondrocyte injury and extracellular matrix degradation.</p>

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From bioinformatic identification to functional validation: MMP25 as a pro-inflammatory mediator in osteoarthritis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月11日

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  • Ting Wu,
  • Jiarui You,
  • Xintong Hao,
  • Shenyi Lu

摘要

Background

Osteoarthritis (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.

Methods

Differentially 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.

Results

Bioinformatics 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.

Conclusion

MMP25 may serve as a potential biomarker for evaluating knee osteoarthritis and it appears to mediate IL-1β-induced chondrocyte injury and extracellular matrix degradation.