For example, miR-155 inhibitors can reduce the oxidative stress-related molecules accumulation and prevent damage to mitochondrial and cardiomyocyte apoptosis through the increasing pathway of nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) signaling, thereby improving diabetic myocardial fibrosis [16]. This evidence concerns the gene HMOX1 and diabetes mellitus.