Its overexpression is associated with improved pressure and glycemic control, reduced oxidative stress and modulation of ER stress [41], prevention of cardiac hypertrophy and fibrosis induced by Ang II [42], and of acute lung injury by the modulation of pro-inflammatory molecules [43], while its loss leads to cardiac dysfunction, hypertrophy, fibrosis and a greater diastolic function [44]. Here, AGT is linked to cardiac hypertrophy.