Abstract
The endothelium is one of the most important, and certainly the most extensive, organs involved in cardiovascular homeostasis. The endothelium-derived vasoactive factors inhibiting smooth muscular cells contraction and proliferation, and platelet function, include nitric oxide (NO), prostacyclin and endothelial-derived hyperpolarizing factor. However, endothelial cells can also produce vasoconstrictive, proaggregant, promitogen mediators, such as thromboxane A2, prostaglandin H2, endothelin 1, and angiotensin II. Therefore, any impairment of endothelial function may trigger the typical chain of events of atherogenesis, characterised by vasoconstriction, cellular proliferation and thrombosis. In this regard, the biological link between endothelial dysfunction and atherosclerosis is a reduced bioavailability of NO. However, the precise mechanisms by which the endothelial dysfunction occurs remain still unclear. A decreased bioavailability of NO can be caused by its enhanced reactive oxygen species (ROS) breakdown. Oxidative stress may represent a common mechanism by which different cardiovascular risk factors cause endothelial dysfunction and trigger atherothrombotic process.
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