Treatment with exendin-4, as a GLP-1R agonist in a MI animal model, decreased the size of the infarcted myocardium, prevented the dilation of cardiac chambers and the progressive remodeling, improved the systolic function of the heart and suppressed myocyte hypertrophy and fibrosis, effects mediated by the circulating GLP-1 and ventricular GLP-1R. This evidence concerns the gene GCG and myocardial infarction.