ArticleCellular and molecular life sciences : CMLS2026
Obesity-induced oleic acid metabolic dysregulation may exacerbate osteoarthritis through the degradation of SOX9.
Article in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Lipid droplet-mitochondria crosstalk in osteoarthritis: linking lipid routing to metabolic mismatch.Frontiers in molecular biosciences · 2026Review
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Authors and funding
13 authors.
Funding
Abstract
Obesity-related osteoarthritis (OA) is a degenerative joint disease accompanied by metabolic disorders. However, the specific metabolites and their molecular mechanisms remain unclear. Here, we establish a mouse model of obesity by feeding a high-fat diet (HFD) and find that HFD feeding promotes articular cartilage degeneration and accelerates OA progression. By using the untargeted metabolomics analysis, we identify oleic acid (OLA), a common monounsaturated fatty acid, as a significantly upregulated metabolite accumulating in articular cartilage. We further show that OLA disrupts extracellular matrix (ECM) homeostasis and promotes ubiquitin-mediated degradation of the key upstream transcription factor sex-determining region Y-type high-mobility group box protein 9 (SOX9) in murine chondrocytes and human cartilage explants. RNA-sequencing and further immunofluorescence staining reveal aberrant activation of Ca2
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