Endothelium-derived nitric oxide tonically inhibits endothelial cell activation, providing a mechanistic link between endothelial dysfunction and the development of atherosclerosis.
The thin layer of cells that lines the interior of blood vessels, known as the endothelium, plays a complex role in vascular biology. The endothelium mediates blood vessel tone, hemostasis, neutrophil recruitment, hormone trafficking, and fluid filtration. Endothelial dysfunction, as defined by a lack of NO, has been linked to a variety of disease states, including atherosclerosis, diabetes mellitus, coronary artery disease, hypertension, and hypercholesterolemia. Indeed, restoration of endothelial function is one of the earliest recognizable benefits of statin therapy. In 1995, James Liao and colleagues published a study in the JCI demonstrating that NO is a vascular protective factor that limits endothelial activation and prevents leukocyte adhesion to the vessel wall.
James K. Liao (Fri,) conducted a editorial in Endothelial dysfunction and vascular disease. Nitric oxide (NO) was evaluated. Endothelium-derived nitric oxide tonically inhibits endothelial cell activation, providing a mechanistic link between endothelial dysfunction and the development of atherosclerosis.