SMOC2 accelerates myocardial fibrosis following myocardial infarction by promoting lipid peroxidation through inhibition of the LKB1/AMPKα/FOXO3 pathway

SMOC2 promotes cardiac injury and fibrosis following MI by suppressing the LKB1/AMPKα/FOXO3 signalling pathway through interaction with integrin αvβ5, thereby enhancing lipid peroxidation and oxidative stress. These findings suggest that targeting SMOC2 or reactivating the AMPKα/FOXO3 axis may serve as a potential therapeutic strategy to mitigate maladaptive cardiac remodeling after myocardial infarction.