NOS3 and endothelial dysfunction: Several studies have reported that, in ECs, the endogenous production of NO at nanomolar concentrations through eNOS activation represents a vasoprotective molecular mechanism of the vascular endothelium, while exaggerated release of NO as a consequence of iNOS activation leads to the rapid reaction of NO with O2●−, generating ONOO−, the main compound responsible for the onset of endothelial dysfunction and, in the late stages, the development of atherothrombosis [67,68,69].