Recently, by using a novel transgenic animal model that overexpression of MnSOD in mouse heart ECs (MHECs), MnSOD promoted ECs proliferation and coronary angiogenesis, protected cardiac function in non-reperfused myocardial infarction by reduction of mtROS, increase of assembly of mitochondrial complexes into supercomplexes, and upregulation of mitochondrial respiration [16]. This evidence concerns the gene SOD2 and myocardial infarction.