The major molecular mechanisms mediating the renoprotective effects of SGLT2 inhibitors: An update

Abstract

The incidence of diabetes mellitus, as well as its complications, is rapidly growing. Diabetic nephropathy is one of the most prevalent disorders induced by chronic uncontrolled hyperglycemia and is accompanied by a reduction in renal sufficiency with microstructural tissue damage in the kidneys. Many therapeutic protocols have been designed to address the treatment and prevention of diabetic nephropathy. Sodium-glucose co-transporter 2 inhibitors (SGLT2i) are a newly introduced class of glucose-lowering agents that reduce blood glucose by inhibition of urinary glucose reabsorption in renal proximal tubules and so induce glycosuria. Also, these hypoglycemic agents may provide protective effects in different tissues such as cardiovascular, brain, and kidneys. In recent years, accumulating evidence has indicated that SGLT2i possess potent renal protective properties in the setting of diabetes. In the current study, we present the latest findings regarding the renoprotective effects of SGLT2 inhibition and discuss the molecular mechanisms involved.

Keywords

• Diabetic nephropathy
• SGLT2
• Kidney
• Oxidative stress
• Hemodynamic changes
• Interleukins