Resistin upregulates fatty acid oxidation in synoviocytes of metabolic syndrome-associated knee osteoarthritis via CAP1/PKA/CREB to promote inflammation and catabolism
Authors' conclusion
This study clarifies the mechanism by which MetS causes synovitis from a metabolic perspective and provides new ideas for further research and treatment of MetS-KOA.
Study context
- Population
- Females with knee OA with or without metabolic syndrome: synovium and fibroblast-like synoviocytes
- Comparison
- Metabolic Syndrome (MetS)-associated knee osteoarthritis (KOA) vs non-MetS-associated KOA synovium and fibroblast-like synoviocytes (FLS)
Main finding
As reported in the abstract
- MetS-KOA-FLS expressed higher inflammatory factors and catabolic enzymes and showed stronger adhesive and invasive ability vs nMetS-KOA-FLS
- Resistin an important factor in serum and internal environment of MetS-KOA patients; mediated the differences in fatty acid oxidation (FAO) between the two groups
- Resistin activated PKA/CREB via CAP1 and upregulated FAO, promoting the inflammatory and catabolic phenotype of MetS-KOA-FLS
Original publication
Resistin upregulates fatty acid oxidation in synoviocytes of metabolic syndrome-associated knee osteoarthritis via CAP1/PKA/CREB to promote inflammation and catabolism. Arthritis Res Ther. Published 29 April 2025. doi:10.
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