Abstract
The development of sodium-glucose transporter 2 inhibitor (SGLT2i) broadens the therapeutic strategies in treating diabetes mellitus. By inhibiting sodium and glucose reabsorption from the proximal tubules, the improvement in insulin resistance and natriuresis improved the cardiovascular mortality in diabetes mellitus (DM) patients. It has been known that SGLT2i also provided renoprotection by lowering the intraglomerular hypertension by modulating the pre- and post- glomerular vascular tone. The application of SGLT2i also provided metabolic and hemodynamic benefits in molecular aspects. The recent DAPA-CKD trial and EMPEROR-Reduced trial provided clinical evidence of renal and cardiac protection, even in non-DM patients. Therefore, the aim of the review is to clarify the hemodynamic and metabolic modulation of SGLT2i from the molecular mechanism.
Highlights
Sodium–glucose cotransporter (SGLT) 2 inhibitors (SGLT2i) are essential in the therapeutic management of diabetic nephropathy
This study reviews the pleiotropic effect of sodium-glucose transporter 2 inhibitor (SGLT2i), in the management of cardiorenal syndrome based on molecular mechanisms
Clinical trials have failed to demonstrate the use of SGLT2i compensatory heart rate (HR) increase [53]. These findings suggest a sympatholytic effect of SGLT2i, which may contribute to the cardioprotective effects of SGLT2i treatment
Summary
Sodium–glucose cotransporter (SGLT) 2 inhibitors (SGLT2i) are essential in the therapeutic management of diabetic nephropathy. Their role in lowering the mortality associated with congestive heart failure and in alleviating the glomerular filtration rate (GFR) decline has been proven by multiple landmark clinical trials. They improve mortality by reducing the sodium and glucose load on the body. This study reviews the pleiotropic effect of SGLT2i, in the management of cardiorenal syndrome based on molecular mechanisms
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have