Abstract
Gliflozins, also known as sodium-glucose transport protein 2 (SGLT2) inhibitors, are a class of oral drugs, integrated as first-line in the treatment of type 2 diabetes mellitus (T2DM), especially in patients with cardiovascular diseases( 1 ). These drugs work through an original mechanism, targeting the SGLT2 and offering distinct advantages over traditional anti-diabetic drugs. Basically, they prevent the reabsorption of glucose from blood filtered by kidneys, leading to increased sodium and glucose excretion in urine. Importantly, even if SGLT2Is had been originally developed to prevent glucose and sodium reabsorption in the kidney, their beneficial effects probably involve extrarenal mechanisms not fully elucidated until now. Beyond direct impact on kidneys, they exert more pleiotropic effects including: 1/ blood glucose levels; 2/ metabolic improvement with weight loss, increased insulin sensitivity and subsequent benefits, 3/ pleiotropic effects on cardiovascular system and kidneys (and their interrelationships). These last effects are depicted as “pleiotropic” and could involve many pathophysiological pathways such as locally tubuloglomerular protection but more systemically: oxidative stress, mitochondrial homeostasis, antiapoptotic properties, sympathetic nervous system inhibition, lower blood pressure, … These basic aspects have been recently reviewed elsewhere( 2 ). As patients with T2DM and/or cardiovascular disease present basic microinflammation( 3 ), anti-inflammatory approaches, even with mildly but sustainable properties are particularly of interest( 4 ). However, the potential vascular impacts of gliflozins had not been extensively studied and deserve to be better understood, as they could represent a common beneficial pathway for many positive clinical impacts depicted above.