Do pleiotropic effects of statins beyond lipid alterations exist in vivo? What are they and how do they differ between statins?

被引：17

作者：

Faggiotto A. ^{[1
]}

Paoletti R. ^{[1
]}

机构：

[1] Institute of Pharmacological Sciences, University of Milan, Via Balzaretti, 9, Milan

来源：

Current Atherosclerosis Reports | 2000年 / 2卷 / 1期

关键词：

Lovastatin; Pleiotropic Effect; Pravastatin; Simvastatin; Statin;

D O I：

10.1007/s11883-000-0091-3

中图分类号：

学科分类号：

摘要：

The inhibition of cellular proliferation, the restoration of endothelial activity, the inhibition of platelet reactivity, and an antioxidant potential are only a few examples of pleiotropic effects of statins. This review analyzes the current knowledge on the pleiotropic properties of this class of drugs and examines the relevant data that support the presence of these effects in vivo. The favorable outcome of major trials of statins has indicated that pleiotropic factors indeed play a role in cardiovascular protection. In addition, recent data indicate that many pleiotropic effects influence mechanisms that belong to the extravascular compartment, as well. Perhaps, some of these properties may eventually justify additional indications for statins and improve the treatment of other diseases, including inflammation and cancer. © 2000, Current Science Inc.

引用

页码：20 / 25

页数：5

共 58 条

[1]

Shepherd J., Cobbe S.M., Ford I., Et al., Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West Of Scotland Coronary Prevention Study Group, N Engl J Med, 333, pp. 1301-1307, (1995)

[2]

Sacks F.M., Pfeffer M.A., Moye L.A., Et al., The effect of pravastatin on coronary events after myocardial infarction in patient with average cholesterol levels, N Engl J Med, 335, pp. 1001-1009, (1996)

[3]

Downs J.R., Clearfield M., Weis S., Et al., Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels. Results of AFCAPS/TexCAPS, JAMA, 279, pp. 1615-1622, (1998)

[4]

Buchwald H., Campos C.T., Boen J.R., Disease-free intervals after partial ileal bypass in patients with coronary heart disease and hypercholesterolemia: report from the program on the surgical control of the hyperlipidemias (POSCH), J Am Coll Cardiol, 26, pp. 351-357, (1995)

[5]

The Lipid Research Clinics Coronary Primary Prevention Trial Results: 1. Reduction in incidence of coronary heart disease, JAMA, 251, pp. 351-364, (1984)

[6]

Laufs U., La Fata V., Plutzky J., Et al., Upregulation of endothelial nitric oxide synthase by HMG CoA reductase inhibitors, Circulation, 97, pp. 1129-1135, (1998)

[7]

Brandes R.P., Behra A., Lebherz C., Et al., Lovastatin maintains nitric oxide—but not EDHF-mediated endothelium-dependent relaxation in the hypercholesterolemic rabbit carotid artery, Atherosclerosis, 142, pp. 97-104, (1999)

[8]

Endres M., Laufs U., Huang Z., Et al., Stroke protection by 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors mediated by endothelial nitric oxide synthase, PNA S, 95, pp. 8880-8885, (1998)

[9]

Hernandez-Perera O., Perez-Sala D., Navarro-Antolin J., Et al., Effects of the 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors, atorvastatin and simvastatin, on the expression of endothelin-1 and endothelial nitric oxide synthase in vascular endothelial cells, J Clin Invest, 101, pp. 2711-2719, (1998)

[10]

Essig M., Nguyen G., Prie D., Et al., 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors increase fibrinolytic activity in rat aortic endothelial cells. Role of geranylgeranylation and Rho proteins, Circ Res, 83, pp. 683-690, (1998)

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