The cardioprotective effects of statins

被引：9

作者：

Eto, M ^{[1
]}

Lüscher, TF ^{[1
]}

机构：

[1] Univ Zurich, Inst Physiol, Univ Hosp & Cardiovasc Res, Ctr Cardiovasc, Zurich, Switzerland

来源：

CORONARY ARTERY DISEASE | 2004年 / 15卷 / 05期

关键词：

statins; ischemia/reperfusion; endothelial nitric oxide synthase;

D O I：

10.1097/01.mca.0000130228.11062.4d

中图分类号：

R5 [内科学];

学科分类号：

1002 [临床医学]; 100201 [内科学];

摘要：

Many large randomized clinical trials have demonstrated that statins are effective in terms of prevention of cardiovascular events. It has been presumed that these beneficial effects could be due to not only improved plasma lipid profiles but also to the direct actions on the vascular wall. In addition to the direct vascular protective effects, several lines of experimental evidence have been accumulated that statins have also cardioprotective effects against ischaemia/reperfusion injury. This effect appears to be a class-effect and activation and up-regulation of eNOS by statins play an important role. (C) 2004 Lippincott Williams Wilkins.

引用

页码：243 / 245

页数：3

共 29 条

[1]

Effect of lipid-lowering therapy on early mortality after acute coronary syndromes: an observational study [J].

Aronow, HD ;

Topol, EJ ;

Roe, MT ;

Houghtaling, PL ;

Wolski, KE ;

Lincoff, AM ;

Harrington, RA ;

Califf, RM ;

Ohman, EM ;

Kleiman, NS ;

Keltai, M ;

Wilcox, RG ;

Vahanian, A ;

Armstrong, PW ;

Lauer, MS .

LANCET, 2001, 357 (9262) :1063-1068

[2]

Atorvastatin, administered at the onset of reperfusion, and independent of lipid lowering, protects the myocardium by up-regulating a pro-survival pathway [J].

Bell, RM ;

Yellon, DM .

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2003, 41 (03) :508-515

[3]

Collins R, 2002, LANCET, V360, P7, DOI 10.1016/S0140-6736(02)09327-3

[4]

Simvastatin reduces reperfusion injury by modulating nitric oxide synthase expression: an ex vivo study in isolated working rat hearts [J].

Di Napoli, P ;

Taccardi, AA ;

Grilli, A ;

Spina, R ;

Felaco, M ;

Barsotti, A ;

De Caterina, R .

CARDIOVASCULAR RESEARCH, 2001, 51 (02) :283-293

[5]

Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation [J].

Dimmeler, S ;

Fleming, I ;

Fisslthaler, B ;

Hermann, C ;

Busse, R ;

Zeiher, AM .

NATURE, 1999, 399 (6736) :601-605

[6]

Statin prevents tissue factor expression in human endothelial cells -: Role of Rho/Rho-kinase and Akt pathways [J].

Eto, M ;

Kozai, T ;

Cosentino, F ;

Joch, H ;

Lüscher, TF .

CIRCULATION, 2002, 105 (15) :1756-1759

[7]

Thrombin suppresses endothelial nitric oxide synthase and upregulates endothelin-converting enzyme-1 expression by distinct pathways -: Role of Rho/ROCK and mitogen-activated protein kinase [J].

Eto, M ;

Barandiér, C ;

Rathgeb, L ;

Kozai, T ;

Joch, H ;

Yang, ZH ;

Lüscher, TF .

CIRCULATION RESEARCH, 2001, 89 (07) :583-590

[8]

Regulation of endothelium-derived nitric oxide production by the protein kinase Akt [J].

Fulton, D ;

Gratton, JP ;

McCabe, TJ ;

Fontana, J ;

Fujio, Y ;

Walsh, K ;

Franke, TF ;

Papapetropoulos, A ;

Sessa, WC .

NATURE, 1999, 399 (6736) :597-601

[9]

HORI Y, 1991, ONCOGENE, V6, P515

[10]

Rosuvastatin, a new HMG-CoA reductase inhibitor, protects ischemic reperfused myocardium in normocholesterolemic rats [J].

Ikeda, Y ;

Young, LH ;

Lefer, AM .

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 2003, 41 (04) :649-656

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