To elucidate the mechanistic roles of Rapgef5 and Ing1 in cardiomyocytes under diabetic myocardial infarction conditions, we investigated the effects of Rapgef5 overexpression and Ing1 knockdown in human cardiomyocytes (AC16) subjected to high glucose and high lipid (HG/HL) conditions in conjunction with hypoxia/reoxygenation. Here, RAPGEF5 is linked to myocardial infarction.