The Dichotomous Role of Nitric Oxide in the Pathogenesis of Accelerated Atherosclerosis Associated with Systemic Lupus Erythematosus

Title: The Dichotomous Role of Nitric Oxide in the Pathogenesis of Accelerated Atherosclerosis Associated with Systemic Lupus Erythematosus

Volume: 4 Issue: 7

Author(s): Marc C. Levesque and J. Brice Weinberg

Affiliation:

Keywords: nitric oxide, inflammation, autoimmunity, endothelium, platelets, macrophages, matrix metalloproteinase 2

Abstract: Atherosclerosis is an inflammatory disorder, and the inflammation associated with systemic lupus erythematosus (SLE) accelerates the development of atherosclerosis. Nitric oxide (NO) is an important mediator of inflammation including the inflammation associated with atherosclerosis and SLE. Endothelial nitric oxide synthase (NOS3)-mediated constitutive expression of NO promotes endothelial integrity and normal vascular function. In contrast, inducible nitric oxide synthase- (NOS2) mediated expression of NO promotes endothelial dysfunction and atherogenesis. Statins appear to have antiinflammatory properties and reverse many of the deleterious effects associated with NO metabolism in atherosclerosis. Statins augment NOS3 expression and inhibit the induction of NOS2. Therefore, the balance between normal vascular function and atherogenesis may be mediated by differences in the quantity, location, and timing of NO production within vessel walls.

Cite this article as:

Levesque C. Marc and Weinberg Brice J., The Dichotomous Role of Nitric Oxide in the Pathogenesis of Accelerated Atherosclerosis Associated with Systemic Lupus Erythematosus, Current Molecular Medicine 2004; 4 (7) . https://dx.doi.org/10.2174/1566524043359872