KDM3A and Hyperglycemia: By establishing hyperglycemia and subsequently intensive GC myocardial injury models both in vitro and in vivo, our experiment provides compelling evidence that KDM3A inhibition could epigenetically modification of NF-K b/P65 by increasing the level of H3K9me2, which consequently ameliorate hyperglycemia-induced persistent myocardial damage and cardiac dysfunction.