Sun and others [19, 56, 57] studied the effects of SalA on endothelial dysfunction and vascular remodeling using disease models including angioplasty-related restenosis, injury-induced neointimal hyperplasia, oxidative stress, and advanced glycation end product- (AGE-) induced endothelial dysfunction through enhancing endothelial nitric oxide synthase (eNOS) and its upstream regulators such as cAMP-related signaling. This evidence concerns the gene NOS3 and endothelial dysfunction.