期刊
CIRCULATION JOURNAL
卷 74, 期 5, 页码 818-826出版社
JAPANESE CIRCULATION SOC
DOI: 10.1253/circj.CJ-10-0110
关键词
Cholesterol; Pleiotropic effects; Rho kinase; Statin; Vascular
资金
- National Institutes of Health [HL052233]
- Deutsche Forschungsgesellschaft [ZH 231/1-1]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL048743, R01HL070274, R01HL080187, R01HL052233] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK062729, R01DK085006] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P01NS010828, R01NS070001] Funding Source: NIH RePORTER
Statins are 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, which are widely used to lower serum cholesterol levels in the primary and secondary prevention of cardiovascular disease. Recent experimental and clinical evidence suggests that the beneficial effects of statins may extend beyond their cholesterol-lowering effects, to include so-called pleiotropic effects. These cholesterol-independent effects include improving endothelial function, attenuating vascular and myocardial remodeling, inhibiting vascular inflammation and oxidation, and stabilizing atherosclerotic plaques. The mechanism underlying some of these pleiotropic effects is the inhibition of isoprenoid synthesis by statins, which leads to the inhibition of intracellular signaling molecules Rho, Rac and Cdc42. In particular, inhibition of Rho and one of its downstream targets, Rho kinase, may be a predominant mechanism contributing to the pleiotropic effects of statins. The aim of the present review is to provide an update on the non-cholesterol-dependent statin effects in the cardiovascular system and highlight some of the recent findings from bench to bedside to support the concept of statin pleiotropy. (Circ J 2010; 74: 818-826)
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