Role of endothelial dysfunction in atherosclerosis

As the major regulator of vascular homeostasis, the endothelium exerts a number of vasoprotective effects, such as vasodilation, suppression of smooth muscle cell growth, and inhibition of inflammatory responses. Many of these effects are largely mediated by nitric oxide, the most potent endogenous...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 2004-06, Vol.109 (23 Suppl 1), p.III27-III32
Main Authors: Davignon, Jean, Ganz, Peter
Format: Article
Language:English
Subjects:
Arteriosclerosis - physiopathology
Coronary Disease - diagnosis
Coronary Disease - epidemiology
Coronary Disease - prevention & control
Coronary Disease - therapy
Endothelium, Vascular - diagnostic imaging
Endothelium, Vascular - physiopathology
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology
Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use
Lipoproteins, LDL - blood
Nitric Oxide - physiology
Nitric Oxide Synthase - metabolism
Nitric Oxide Synthase Type III
Oxidative Stress
Risk Factors
Signal Transduction
Treatment Outcome
Ultrasonography
Vasoconstriction
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Summary:As the major regulator of vascular homeostasis, the endothelium exerts a number of vasoprotective effects, such as vasodilation, suppression of smooth muscle cell growth, and inhibition of inflammatory responses. Many of these effects are largely mediated by nitric oxide, the most potent endogenous vasodilator. Nitric oxide opposes the effects of endothelium-derived vasoconstrictors and inhibits oxidation of low-density lipoprotein. A defect in the production or activity of nitric oxide leads to endothelial dysfunction, signaled by impaired endothelium-dependent vasodilation. Accumulating evidence suggests that endothelial dysfunction is an early marker for atherosclerosis and can be detected before structural changes to the vessel wall are apparent on angiography or ultrasound. Many of the risk factors that predispose to atherosclerosis can also cause endothelial dysfunction, and the presence of multiple risk factors has been found to predict endothelial dysfunction. A number of clinical trials have shown that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) improve endothelial dysfunction in patients with coronary risk factors beyond what could be attributed to their impact on plasma lipids. Studies have elucidated several possible mechanisms by which statin therapy may improve endothelial dysfunction, including upregulation of nitric oxide production or activity and reduction of oxidative stress.
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.0000131515.03336.f8