SGLT2 inhibitors protect cardiomyocytes from myocardial infarction: a direct mechanism?

SGLT2 inhibitors have been developed as a novel class of glucose-lowering drugs affecting reabsorption of glucose and metabolic processes. They have been recently identified to be remarkably favorable in treating cardiovascular diseases, especially heart failure. Preclinical experiments have shown that SGLT2 inhibitors could hinder the progression of myocardial infarction and alleviate cardiac remodeling by mechanisms of metabolism influence, autophagy induction, inflammation attenuation and fibrosis reduction. Here we summarize the direct mechanism of SGLT2 inhibitors on myocardial infarction and investigate whether it could be applied to the clinic in improving cardiac function and healing after myocardial infarction.Inhibitors of the protein SGLT2, including empagliflozin and dapagliflozin, are some of the most efficient glucose-lowering drugs used for the treatment of diabetes. In recent years, researchers and clinicians have found that SGLT2 inhibitors could also be applied in the treatment of some cardiovascular diseases. Every year, a number of people, especially the elderly and disabled, experience the pain of myocardial infarction (‘heart attack’). Preclinical experiments have shown that SGLT2 inhibitors could hinder the progression of myocardial infarction. Some clinical trials have shown the same result. Hence, in the near future, SGLT2 inhibitors promise to be used as effective drugs in treating myocardial infarction.