© 2001 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Vascular effects of HMG CoA-reductase inhibitors (statins) unrelated to cholesterol lowering: new concepts for cardiovascular disease
aDepartment of Physiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107, USA
bDepartment of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport, LA 71130, USA
* Corresponding author. Tel.: +1-215-503-7760; fax: +1-215-503-2073 allan.m.lefer@mail.tju.edu
Received 21 August 2000; accepted 11 October 2000
KEYWORDS Cholesterol; Lipid metabolism
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| 1 Introduction |
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In 1976, Endo et al. [1] reported on the discovery of a specific competitive inhibitor of the enzyme 3-hydroxy-3-methylglutaryl (HMG) CoA reductase. This compound, isolated from fungi, was called mevastatin. In 1988, Alberts [2] described a more potent HMG CoA reductase inhibitor, lovastatin, isolated from Aspergillus terreus. These two compounds started the development of a series of cholesterol lowering agents, now commonly called statins. Statins block the conversion of HMG CoA to mevalonic acid and thus dramatically attenuate the biosynthesis of cholesterol. These effects occur largely in the liver, where the statins primarily distribute [2]. The major effect of these pharmacologic agents is a marked reduction in LDL-cholesterol levels in the blood.
On the basis of these and other findings, the statins have been widely prescribed in humans with elevated serum cholesterol levels. These statins are well tolerated, are very safe, and effectively lower serum LDL-cholesterol levels and
| 2 Endothelial dysfunction |
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| 3 Key cardiovascular actions of the statins |
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| 4 Statins enhance NO Production |
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| 5 Effects of statins on leukocyte–endothelial interactions |
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| 6 Other potential vasculoprotective and cytoprotective actions of statins |
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| 7 Potential usefulness of statins in other cardiovascular disorders |
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| 8 Summary |
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