Human Acyl-CoA:Cholesterol acyltransferase (ACAT) and its potential as a target for pharmaceutical intervention against atherosclerosis

被引:45
|
作者
Chang, C [1 ]
Dong, RH
Miyazaki, A
Sadashita, N
Zhang, Y
Liu, J
Guo, M
Li, BL
Chang, TY
机构
[1] Dartmouth Med Sch, Dept Biochem, Hanover, NH 03755 USA
[2] Showa Univ, Sch Med, Dept Biochem, Tokyo 142, Japan
[3] Kumamoto Univ, Sch Med, Dept Pathol, Kumamoto 860, Japan
[4] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, State Key Lab Mol Biol, Shanghai 200031, Peoples R China
关键词
acyl-CoA; cholesterol acyltransferase; cholesterol; cholesteryl ester; atherosclerosis;
D O I
10.1111/j.1745-7270.2006.00154.x
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
Acyl-CoA:cholesterol acyltransferase (ACAT) catalyzes the formation of cholesteryl esters from cholesterol and long-chain fatty-acyl-coenzyme A. At the single-cell level, ACAT serves as a regulator of intracellular cholesterol homeostasis. In addition, ACAT supplies cholesteryl esters for lipoprotein assembly in the liver and small intestine. Under pathological conditions, the accumulation of cholesteryl esters produced by ACAT in macrophages contributes to foam cell formation, a hallmark of the early stage of atherosclerosis. Several reviews addressing various aspects of ACAT and ACAT inhibitors are available [1-8]. This review briefly outlines the current knowledge on the biochemical properties of human ACATs, and then focuses on discussing the merit of ACAT as a drug target for pharmaceutical interventions against atherosclerosis.
引用
收藏
页码:151 / 156
页数:6
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