NR3C2 and glomerulosclerosis: Inhibition of the RAAS by ACE inhibition, AT1 receptor blockade (ARB), and MR antagonism is renoprotective in reducing renal injury and suppressing NOX/ROS activity, glomerular capillary pressure, proteinuria, profibrotic TGF-β1 signaling, podocyte abnormalities, glomerular sclerosis inhibit compensatory renal growth [39,40].