SAT1 promotes the progression of OA by regulating TRIM33-mediated p53 acetylation to enhance ferroptosis

In summary, our data indicate that SAT1 is a potential key gene in OA, revealing the crucial role of the SAT1-TRIM33-p53 axis in OA pathogenesis. This axis promotes ferroptosis by enhancing p53 acetylation, suggesting that targeting SAT1 may represent a novel therapeutic strategy for improving OA.