Perspectives on the cardioprotective effects of statins

被引:12
作者
Luo, JD
Chen, AF
机构
[1] Michigan State Univ, Dept Pharmacol & Toxicol, E Lansing, MI 48824 USA
[2] Michigan State Univ, Program Neurosci, E Lansing, MI 48824 USA
关键词
cardiovascular disease; G proteins; inflammation; nitric oxide; oxidative stress; statins; HMG-CoA reductase; heart;
D O I
10.2174/0929867033457205
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Statins are inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase), the rate-limiting enzyme of cholesterol synthesis. In recent years, statins have become the major choice of treatment for hypercholesterolemia. Emerging evidence from both animal and human studies indicates that mechanisms independent of cholesterol lowering effects contribute to the observed clinical benefits of statins. The anti-hypertrophy effect of statins on the cardiac tissue represents one of such mechanisms. The beneficial effects of statins on cardiac hypertrophy and cardioprotection may be attributed to their functional influences on small G proteins such as Ras and Rho, resulting in an increase of endogenous nitric oxide (NO), reduction of oxidative stress, inhibition of inflammatory reaction, and decrease of the renin-angiotensin system activity as well as C-reactive protein (CRP) levels in cardiac tissues. Recent findings from in vitro and in vivo studies of statins on cardioprotective effects are summarized in this review. The unveiled novel mechanisms support the use of statins as the new mainstay therapeutic agents for various cardiovascular diseases and complications.
引用
收藏
页码:1593 / 1601
页数:9
相关论文
共 123 条
[11]   DEMONSTRATION OF FREE-RADICAL GENERATION IN STUNNED MYOCARDIUM OF INTACT DOGS WITH THE USE OF THE SPIN TRAP ALPHA-PHENYL N-TERT-BUTYL NITRONE [J].
BOLLI, R ;
PATEL, BS ;
JEROUDI, MO ;
LAI, EK ;
MCCAY, PB .
JOURNAL OF CLINICAL INVESTIGATION, 1988, 82 (02) :476-485
[12]   DIRECT EVIDENCE THAT OXYGEN-DERIVED FREE-RADICALS CONTRIBUTE TO POSTISCHEMIC MYOCARDIAL DYSFUNCTION IN THE INTACT DOG [J].
BOLLI, R ;
JEROUDI, MO ;
PATEL, BS ;
DUBOSE, CM ;
LAI, EK ;
ROBERTS, R ;
MCCAY, PB .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (12) :4695-4699
[13]   NITRIC-OXIDE ATTENUATES CARDIAC MYOCYTE CONTRACTION [J].
BRADY, AJB ;
WARREN, JB ;
POOLEWILSON, PA ;
WILLIAMS, TJ ;
HARDING, SE .
AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 265 (01) :H176-H182
[14]   Hypertriglyceridemia: A review of clinical relevance and treatment options: Focus on cerivastatin [J].
Breuer, HWM .
CURRENT MEDICAL RESEARCH AND OPINION, 2001, 17 (01) :60-73
[15]   A RECEPTOR-MEDIATED PATHWAY FOR CHOLESTEROL HOMEOSTASIS [J].
BROWN, MS ;
GOLDSTEIN, JL .
SCIENCE, 1986, 232 (4746) :34-47
[16]  
BROWN MS, 1978, J BIOL CHEM, V253, P1121
[17]   Cardiac failure in transgenic mice with myocardial expression of tumor necrosis factor-α [J].
Bryant, D ;
Becker, L ;
Richardson, J ;
Shelton, J ;
Franco, F ;
Peshock, R ;
Thompson, M ;
Giroir, B .
CIRCULATION, 1998, 97 (14) :1375-1381
[18]   Therapeutic strategies to reduce TNF-α mediated cardiac contractile depression following ischemia and reperfusion [J].
Cain, BS ;
Harken, AH ;
Meldrum, DR .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1999, 31 (05) :931-947
[19]   PROTEIN LIPIDATION IN CELL SIGNALING [J].
CASEY, PJ .
SCIENCE, 1995, 268 (5208) :221-225
[20]   C-REACTIVE PROTEIN INDUCES HUMAN PERIPHERAL-BLOOD MONOCYTES TO SYNTHESIZE TISSUE FACTOR [J].
CERMAK, J ;
KEY, NS ;
BACH, RR ;
BALLA, J ;
JACOB, HS ;
VERCELLOTTI, GM .
BLOOD, 1993, 82 (02) :513-520