Micro circulation as a target for the anti-inflammatory properties of statins

被引:29
作者
Scalia, R [1 ]
Stalker, T [1 ]
机构
[1] Thomas Jefferson Univ, Jefferson Med Coll, Dept Physiol, Philadelphia, PA 19107 USA
关键词
cholesterol; nitric oxide; microcirculation; adhesion molecules; endothelium; leukocytes;
D O I
10.1038/sj.mn.7800168
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Statins are inhibitors of the 3-hydroxy-3-methylglutaryl coenzyme A reductase. a ubiquitous enzyme critical for the biosynthesis of cholesterol. Because of their cholesterol-lowering properties, statins are extensively used in medical practice. and large clinical trials have shown that statins effectively reduce cardiovascular related morbidity and mortality. In the past 5 years. all important. new concept suggesting that the cardioprotective effects of statins are not necessarily related to cholesterol-lowering actions ha, emerged. Indeed. in vivo findings have clearly shown that statins exert anti-inflammatory and immunomodulatory effects and that they modulate vascular remodeling under normocholesterolemic conditions. These pleiotropic properties of statins affect important molecules in vascular biology and help preserve endothelial function in acute and chronic inflammatory states of the cardiovascular system including corollary and cerebral artery diseases, diabetes. and atherosclerosis. Emerging evidence indicates that the microcirculation is a crucial target for the pleiotropic actions of statins because of its important role in regulating blood flow, leukocyte-endothelium interactions. and vascular remodeling. Accordingly, this review focuses on the role that the microcirculation plays in the vascular protective action of statins.
引用
收藏
页码:431 / 442
页数:12
相关论文
共 108 条
[1]  
Amerongen GPV, 2000, CIRCULATION, V102, P2803
[2]   Mevastatin, an HMG-CoA reductase inhibitor, reduces stroke damage and upregulates endothelial nitric oxide synthase in mice [J].
Amin-Hanjani, S ;
Stagliano, NE ;
Yamada, M ;
Huang, PL ;
Liao, JK ;
Moskowitz, MA .
STROKE, 2001, 32 (04) :980-985
[3]   Isolation of putative progenitor endothelial cells for angiogenesis [J].
Asahara, T ;
Murohara, T ;
Sullivan, A ;
Silver, M ;
vanderZee, R ;
Li, T ;
Witzenbichler, B ;
Schatteman, G ;
Isner, JM .
SCIENCE, 1997, 275 (5302) :964-967
[4]   Bone marrow origin of endothelial progenitor cells responsible for postnatal vasculogenesis in physiological and pathological neovascularization [J].
Asahara, T ;
Masuda, H ;
Takahashi, T ;
Kalka, C ;
Pastore, C ;
Silver, M ;
Kearne, M ;
Magner, M ;
Isner, JM .
CIRCULATION RESEARCH, 1999, 85 (03) :221-228
[5]   Relation of markers of inflammation (C-reactive protein, fibrinogen, von Willebrand factor, and leukocyte count) and statin therapy to long-term mortality in patients with angiographically proven coronary artery disease [J].
Bickel, C ;
Rupprecht, HJ ;
Blankenberg, S ;
Espiniola-Klein, C ;
Schlitt, A ;
Rippin, G ;
Hafner, G ;
Treude, R ;
Othman, H ;
Hofmann, KP ;
Meyer, J .
AMERICAN JOURNAL OF CARDIOLOGY, 2002, 89 (08) :901-908
[6]   MOLECULAR DETERMINANTS OF SHEAR RATE-DEPENDENT LEUKOCYTE ADHESION IN POSTCAPILLARY VENULES [J].
BIENVENU, K ;
GRANGER, DN .
AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 264 (05) :H1504-H1508
[7]  
BITTERMAN H, 1988, P SOC EXP BIOL MED, V188, P265
[8]  
Blake Gavin J, 2000, Curr Control Trials Cardiovasc Med, V1, P161, DOI 10.1186/CVM-1-3-161
[9]   Novel clinical markers of vascular wall inflammation [J].
Blake, GJ ;
Ridker, PM .
CIRCULATION RESEARCH, 2001, 89 (09) :763-771
[10]   Mechanisms of amelioration of glucose-induced endothelial dysfunction following inhibition of protein kinase C in vivo [J].
Booth, G ;
Stalker, TJ ;
Lefer, AM ;
Scalia, R .
DIABETES, 2002, 51 (05) :1556-1564