It was expected to provide injured cardiomyocytes with more bioenergy via in situ glycolysis improving, regulate the inflammatory and oxidative microenvironment and inhibit cardiac fibrosis arising from EndoMT caused by abundant TGF-β1 cytokines, which would promote the cardiac functions and attenuate the adverse left ventricular remodeling synergistically in an acute MI model. This evidence concerns the gene TGFB1 and myocardial infarction.