NOS3 and endothelial dysfunction: Experimental studies have verified multiple biological responses triggered by Hcy during the process of atherosclerosis, for example, Hcy inhibits glutathione peroxidase to stimulate the proliferation of smooth muscle cells, by which endothelial nitric oxide synthase (eNOS) can be suppressed via the asymmetric dimethyl-L-arginine (ADMA) pathway, leading to endothelial dysfunction and vascular spasms26,56–58.