What is more, mineralocorticoid receptors and RAAS activation are important determinants of post-MI LV dysfunction; specifically, according to a study in mice, deletion of mineralocorticoid receptors in Vascular smooth muscle cells (VSMCs) could ameliorate LV dysfunction post-MI through control of coronary flow reserve and improvement of endothelial function [140]. Here, NR3C2 is linked to myocardial infarction.