TGFB1 and Myocardial fibrosis: In addition, Ang II can activate nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, a main source of endogenous reactive oxygen species (ROS), resulting in a significant increase of intracellular ROS [10], which mediates myocardial fibrosis by stimulating TGF-β1 secretion and promoting cardiac fibroblasts proliferation and collagen synthesis [11].