ArticleJournal of orthopaedic surgery and research2026
IMMT downregulation promotes osteoarthritis development by inducing mitochondrial dysfunction.
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
objectiveThis study aimed to identify key mitochondria-related genes involved in the pathogenesis of osteoarthritis (OA).
methodsPublicly available OA-related gene expression datasets were analyzed. Differential expression analysis, immune infiltration analysis, weighted gene co-expression network analysis (WGCNA), and machine learning were used to identify hub differentially expressed mitochondria-related genes (DE-MRGs) for constructing a molecular signature to predict OA risk. In addition, a nomogram, protein-protein interaction (PPI) network, gene set enrichment analysis (GSEA), and a competing endogenous RNA (ceRNA) network of signature DE-MRGs were generated to assess their predictive performance and regulatory mechanisms in OA. The expression of signature DE-MRGs was validated in interleukin (IL)-1β-treated chondrocytes, and the effects of IMMT knockdown on OA pathogenesis and mitochondrial dysfunction were investigated in vitro.
resultsA molecular signature comprising seven DE-MRGs (IMMT, LONP1, TUFM, SOD2, CYCS, CAT, and DLD) demonstrated high predictive performance for OA. The nomogram established using these genes also exhibited high predictive accuracy for OA risk. Furthermore, GSEA revealed that IMMT was implicated in pathways such as Notch signaling. A ceRNA network involving MEG3-miR-370-3p-IMMT was predicted. Quantitative PCR confirmed significant downregulation of IMMT, TUFM, CAT, and DLD in IL-1β-treated chondrocytes. Knockdown of IMMT promoted OA development and induced mitochondrial dysfunction in chondrocytes.
conclusionThe identified DE-MRG signature holds significant potential for predicting OA. The downregulation of IMMT may contribute to OA pathogenesis by inducing mitochondrial dysfunction. These findings provide a foundation for developing more effective diagnostic and therapeutic strategies for OA.
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