In the MI scenario, heme oxygenase (hmox1) has been demonstrated to reduce infarct size and left ventricular remodeling in murine models of permanent ischemia [19], and exert cardioprotective effects via attenuating cardiomyocyte senescence [20], whereas midkine (mdk) administration prevents left ventricular remodeling by promoting angiogenesis and reducing collagen deposition and apoptosis activation [21]. This evidence concerns the gene HMOX1 and myocardial infarction.