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.