High density lipoproteins and arteriosclerosis - Role of cholesterol efflux and reverse cholesterol transport

被引:584
作者
von Eckardstein, A
Nofer, JR
Assmann, G
机构
[1] Univ Munster, Zent Lab, Inst Klin Chem & Lab Med, D-48129 Munster, Germany
[2] Univ Munster, Inst Arterioskleroseforsch, D-4400 Munster, Germany
关键词
apolipoproteins; lipid transfer proteins; lipases; ABC transporter; Tangier disease;
D O I
10.1161/01.ATV.21.1.13
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
High density lipoprotein (HDL) cholesterol is an important risk factor for coronary heart disease, and HDL exerts various potentially antiatherogenic properties, including the mediation of reverse transport of cholesterol from cells of the arterial wall to the liver and steroidogenic organs. Enhancement of cholesterol efflux and of reverse cholesterol transport (RCT) is considered an important target for antiatherosclerotic drug therapy. Levels and composition of HDL subclasses in plasma are regulated by many factors, including apolipoproteins, lipolytic enzymes, lipid transfer proteins, receptors, and cellular transporters. In vitro experiments as well as genetic family and population studies and investigation of transgenic animal models have revealed that HDL cholesterol plasma levels do not necessarily reflect the efficacy and antiatherogenicity of RCT. Instead, the concentration of HDL subclasses, the mobilization of cellular lipids for afflux, and the kinetics of HDL metabolism are important determinants of RCT and the risk of atherosclerosis.
引用
收藏
页码:13 / 27
页数:15
相关论文
共 216 条
[31]  
CASTLE CK, 1991, J LIPID RES, V32, P439
[32]   Acyl-coenzyme A: Cholesterol acyltransferase [J].
Chang, TY ;
Chang, CCY ;
Cheng, D .
ANNUAL REVIEW OF BIOCHEMISTRY, 1997, 66 :613-638
[33]   Sterol regulatory element binding protein-1 activates the cholesteryl ester transfer protein gene in vivo but is not required for sterol up-regulation of gene expression [J].
Chouinard, RA ;
Luo, Y ;
Osborne, TF ;
Walsh, A ;
Tall, AR .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (35) :22409-22414
[34]  
CHRISTISON JK, 1995, J LIPID RES, V36, P2017
[35]   Hepatic lipase: new insights from genetic and metabolic studies [J].
Cohen, JC ;
Vega, GL ;
Grundy, SM .
CURRENT OPINION IN LIPIDOLOGY, 1999, 10 (03) :259-267
[36]   Reduced aortic lesions and elevated high density lipoprotein levels in transgenic mice overexpressing mouse apolipoprotein A-IV [J].
Cohen, RD ;
Castellani, LW ;
Qiao, JH ;
VanLenten, BJ ;
Lusis, AJ ;
Reue, K .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 99 (08) :1906-1916
[37]  
Collet X, 1999, J LIPID RES, V40, P1185
[38]   Comparison of class B scavenger receptors, CD36 and scavenger receptor BI (SR-BI), shows that both receptors mediate high density lipoprotein-cholesteryl ester selective uptake but SR-BI exhibits a unique enhancement of cholesteryl ester uptake [J].
Connelly, MA ;
Klein, SM ;
Azhar, S ;
Abumrad, NA ;
Williams, DL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (01) :41-47
[39]   Hepatic lipase deficiency [J].
Connelly, PW ;
Hegele, RA .
CRITICAL REVIEWS IN CLINICAL LABORATORY SCIENCES, 1998, 35 (06) :547-572
[40]  
Costet P, 2000, J BIOL CHEM, V275, P28240