SGLT-2 Inhibitors: Ideal Remedy for Cardioprotection in Diabetes Mellitus

Abstract

A chronic metabolic disease, diabetes mellitus (DM), is associated with various comorbidities that considerably decrease the quality of life. Sodium glucose linked transporter 2 (SGLT2) receptors are mainly situated in the proximal tubule of nephron. About 90% of glucose concentration is reabsorbed by these receptors in the nephron. The advanced remedy for the management of DM is sodium glucose co-transporter 2 inhibitors (SGLT2-Is), which inhibits or lowers the reabsorption of glucose. Furthermore, SGLT2-Is enhance the elimination of glucose level in urine (glycosuria). Empagliglozin, canagliflozin, ertugliflozin and dapagliflozin are the standard medications which have been authorized recently, for the management of DM by The Food and Drug Administration (FDA). Besides, having optimistic efficacy to attenuate blood glucose level, these medications have exhibited impressive cardioprotective and renoprotective effects in major clinical trials. Unlike other hypoglycaemic medications, it is found that these agents help in a consistent reduction in hospitalization, due to heart failure with probably multifactorial mechanisms. The cardioprotective efficacy of SGLT2-Is is characterized by enhancement in ventricular loading condition, in metabolism of cardiac cell, adipokines alteration, cardiac fibrosis, and reduction in the necrosis of cardiac cell. Recently confirmed results depict that dapagliflozin gradually decreases the frequency of co-morbidity and mortality in heart failure patients. The present review explores the mechanistic principle and the clinical trial data of SGLT2-Is, which further support cardioprotective effects associated with these medications.

Keywords: SGLT2-Is; canaglifozin; dapagliflozin; diabetes mellitus.; empagliflozin; ertugliflozin.