In this study, through the elderly ischemic model in-vivo and vitro experiments, our results confirmed that the addition of exogenous Wnt3a to elderly mice could effectively reduce the myocardial infarct area, improve heart microcirculation, and reduce the apoptotic cardiomyocytes in the infarcted myocardium, and improved the structure and function of infarcted mice. The gene discussed is WNT3A; the disease is myocardial infarction.