During MI, ischemia and healing cardiac tissue trigger a cascade of signaling reactions involving an increase in reactive oxygen species (ROS) and intracellular Ca2+ levels, a dysregulation of endothelial NO synthase (eNOS) [5,6,7], and the activation of hypoxia-induced factor 1α (HIF-1α) required for blood vessels formation from pre-existing vasculature, an action carried out by endothelial cells (ECs) known as angiogenesis [8], as summarized in Figure 1. Here, NOS3 is linked to myocardial infarction.