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

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

Journal Name: Current Molecular Medicine

Volume 4 , Issue 7 , 2004

Become EABM
Become Reviewer

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.

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

Rights & PermissionsPrintExport Cite as

Article Details

VOLUME: 4
ISSUE: 7
Year: 2004
Page: [777 - 786]
Pages: 10
DOI: 10.2174/1566524043359872
Price: $58

Article Metrics

PDF: 1