NR3C2 and Myocardial fibrosis: Inhibition of aldosterone synthase (ASI) could reduce both MR-dependent (Na+/K+- or Na+/H+- pump activation) and MR-independent (protein kinase C or c-Jun N-terminal kinases activation) deleterious aldosterone effects, such as inflammation, vascular smooth muscle cell hypertrophy, vascular fibrosis, interstitial fibrosis of the kidney, and myocardial fibrosis and hypertrophy [5].