We investigated the function and mechanism of SF3A2 acetylation in heart infarction- and isoproterenol-induced pathological remodeling murine models to discover a theoretical basis for targeted treatment. Cardiomyocytes-specific mutation with adeno-associated virus 9 (AAV9) vector SF3A2-K174R or SF3A2-K174Q models combined with metabolomics, lipidomics,13C-glucose tracing, acetylomics were used to demonstrate mechanisms of SIRT7-mediated deacetylation of SF3A2-K10 in cardiac remodeling.