New insights into the molecular mechanisms of SGLT2 inhibitors on ventricular remodeling

Ventricular remodeling is a pathological process of ventricular response to continuous stimuli such as pressure overload, ischemia or ischemia–reperfusion, which can lead to the change of cardiac structure and function structure, which is central to the pathophysiology of heart failure (HF) and is an established prognostic factor in patients with HF. Sodium glucose cotransporter 2 inhibitors (SGLT2i) get a new hypoglycemic drug that inhibit sodium glucose coconspirator on renal tubular epithelial cells. Recently, clinical trials increasingly and animal experiments increasingly have shown that SGLT2 inhibitors have been largely applied in the fields of cardiovascular diseases, for instance heart failure, myocardial ischemia–reperfusion injury, myocardial infarction, atrial fibrillation, metabolic diseases such as obesity, diabetes cardiomyopathy and other diseases play a cardiovascular protective role in addition to hypoglycemic. These diseases are association with ventricular remodeling. Inhibiting ventricular remodeling can improve the readmission rate and mortality of patients with heart failure. So far, clinical trials and animal experiments demonstrate that the protective effect of SGLT2 inhibitors in the cardiovascular field is bound to inhibit ventricular remodeling. Therefore, this review briefly investigates the molecular mechanisms of SGLT2 inhibitors on ameliorating ventricular remodeling, and further explore the mechanisms of cardiovascular protection of SGLT2 inhibitors, in order to establish strategies for ventricular remodeling to prevent the progress of heart failure.