https://www.selleckchem.com/pr....oducts/enarodustat.h
In the mouse model, adenoviral RIP3 overexpression accelerated cartilage disruption, whereas depletion reduced DMM-induced OA pathogenesis. Additionally, TRIM24 knockdown upregulated RIP3 expression; its downregulation promoted OA pathogenesis in knee joint tissues. The CMap approach and in silico binding assay identified AZ-628 as a potent RIP3 inhibitor and demonstrated that it abolished RIP3-mediated OA pathogenesis by inhibiting RIP3 kinase activity. TRIM24-RIP3 axis perturbation promotes OA chronicity by activating RIP3 kinase,
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