Oxidative stress and cardiovascular disease

The endothelium is one of the most important, and certainly the most extensive, organs involved in cardio- vascular 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 impair- ment of endothelial function may trigger the typical chain of events of atherogenesis, characterised by vasocon- striction, 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.