Abstract
Heart failure (HF) is a serious problem in a modern world, with increasing prevalence among ageing populations. The use of sodium-glucose cotransporter-2 (SGLT2) inhibitors, originally intended to treat type 2 diabetes, has revolutionised the treatment of HF. In this review article, we present the latest evidence on the mechanism of action of SGLT2 inhibitors, also called flosins, in HF. The primary mechanism of action of flosins is to reduce glucose reabsorption from glomerular filtration in the proximal renal tubule with a concomitant reduction in sodium reabsorption, leading to urinary glucose excretion and osmotic diuresis. Based on experimental findings, several pleiotropic effects of SGLT2 inhibitors have been proposed. Mechanisms also include regulation of inflammatory and oxidative pathways along with improved endothelial function. Recent multicentre studies of SGLT2 inhibitors have shown that they reduce hospitalisations for heart failure after their use, regardless of type 2 diabetes and the degree of cardiac systolic dysfunction.
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