ABSTRACT
Atherosclerosis is the most common form of vascular disease, causing morphologic disruption of the blood vessel wall that includes lipid deposition, vascular smooth muscle proliferation, and fibrosis. Atherosclerosis begins when the endothelium’s protective properties are overcome by injurious factors such as high cholesterol, tobacco smoke, diabetes mellitus, and high blood pressure. One of the first steps in atherogenesis is the expression of leukocyte adhesion molecules, such as intercellular adhesion molecule–1 (ICAM-1) and vascular cell adhesion molecule–1 (VCAM-1), on the endothelial surface. These molecules, along with chemokines such as monocyte chemoattractant protein–1 (MCP-1), facilitate the capture and migration of leukocytes from circulating blood into the vascular wall. Multiple mechanisms may contribute to endothelial dysfunction and reduce the bioavailability of NO by decreasing its synthesis or increasing its degradation. The importance of superoxide anion as a cause of endothelial dysfunction can be inferred from studies that have examined the effect of antioxidants on endothelium-dependent vasorelaxation.
