Advances in early reperfusion therapies focused on the revascularization of the ischemic tissues, in the last decades, lead to reduced mortality in acute myocardial infarction (MI) patients. However, a large proportion of patients show inadequate myocardial perfusion because of dysfunction of the microcirculation. The high prevalence of microvascular dysfunction after reperfusion therapies and the negative prognostic of this procedure justify the search for therapeutic strategies that aim to restore the microvascular network. It is well known that the size of the initial infarct, the duration of ischemia and the efficiency of reperfusion determine myocardial tissue damage and cardiomyocyte loss after myocardial infarction. Therefore any advancement on the mechanisms that induce the repair process of microvascular dysfunction after reperfused MI is of great interest. Here, we will review the different proteins and cells known to participate in angiogenesis induction post-MI and we will also discuss the potential pharmacological and cellular processes that promote the recovery of microvasculature by angiogenesis stimulation after MI.