Atherosclerotic cardiovascular disease remains globally the main cause of death and morbidity. The underlying mechanism of atherogenesis is multifactorial, involving functional changes of vascular cells including endothelial cells, smooth muscle cells, adventitial, and perivascular cells, and circulating cells including platelets and inflammatory cells. Clinical studies demonstrate that endothelial dysfunction reflected by decreased bioavailability of endothelial nitric oxide (NO) derived from endothelial NO-synthase (eNOS) is not only associated with atherosclerosis and risk factors such as hypercholesterolemia, diabetes, advanced age, etc, but also predicts the future clinical outcomes of patients. The firm evidence for the role of eNOS in anti-atherogenesis stems from earl
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