SGK1 and endothelial dysfunction: Meanwhile, Hcy undergoes oxidative reactions in vivo to generate ROS and activate epithelial sodium channels, which induce endothelial dysfunction through reactive oxygen species (ROS)/COX-2-dependent activation of SGK-1/Nedd4-2 (serum/glucocorticoid-regulated kinase 1/neural precursor cell expression of developmentally down-regulated protein 4-2) signaling (88), and cause NO production and release is inhibited, leading to increased cellular damage effects such as lipid peroxidation and ultimately endometrial vascularization.