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Eukaryotic cells face constantly the formation of reactive oxygen species (ROS) as a result of their aerobic metabolism. ROS play an important role in the regulation of signal transduction pathways and gene expression but its over-production is acutely harmful to cells, particularly in cardiovascular diseases (CVD) by a mechanism that is not fully understood. Most CVD (the leading cause of mortality in developed countries) entail the focal development of atherosclerotic plaques in response to various deleterious insults that affect the artery wall’s cells (Simionescu, 2007). Atheroma may occlude partially or totally the arterial lumen and ultimately, rupture of the vulnerable plaques results in thrombus formation and obstruction of the vessels of vital organs like heart, brain, lung, and kidney. Atheroma formation is characterized by progressive lipid accumulation in the vessel’s intima, dysfunctions of endothelial cells (EC) and smooth muscle cells (SMC), and a strong inflammatory reaction with the participation of extravasated immune cells (Fearon & Faux, 2009). Compelling evidence (including ours) revealed that oxidative stress and NADPH oxidase derived ROS play the key role in all stages of atherosclerosis and that genetic ablation of various oxidase components protects the cells against the detrimental effects of oxidative stress (Simionescu et al., 2009). Therefore, understanding the molecular mechanisms of ROS formation and function is a prerequisite of an effective anti-oxidative stress therapy.

Vascular Biology of Reactive Oxygen Species and NADPH Oxidases: Role in Atherogenesis