Aldosterone-induced oxidative stress and inflammation can promote endothelial dysfunction and increase the expression of pro-fibrotic molecules, such as transforming growth factor-β1 (TGF-β1), connective tissue growth factor (CTGF), placental growth factor (PGF), endothelin 1 (ET1), osteopontin and galectin-3, eventually leading to fibrosis in the heart, kidney and vasculature [88]. The gene discussed is EDN1; the disease is endothelial dysfunction.