CD226 and myocardial infarction: Here, we demonstrate that CD226 expression is remarkably increased in the infarcted heart after MI, and CD226 deletion favors macrophages activation status toward reparative phenotype in the ischemic heart, while restraining inflammatory monocytes mobilization from the spleen and peripheral blood, leading to increased reparative collagen deposition and angiogenesis, thereby contributing to infarct healing and preserved cardiac function.