Open AccessHuman Acyl‐CoA:cholesterol Acyltransferase (ACAT) and its Potential as a Target for Pharmaceutical Intervention against Atherosclerosis
Author(s) -
CHANG Catherine,
DONG Ruhong,
MIYAZAKI Akira,
SAKASHITA Naomi,
ZHANG Yi,
LIU Jay,
GUO Michael,
LI BoLiang,
CHANG TaYuan
Publication year - 2006
Publication title -
acta biochimica et biophysica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.771
H-Index - 57
eISSN - 1745-7270
pISSN - 1672-9145
DOI - 10.1111/j.1745-7270.2006.00154.x
Subject(s) - sterol o acyltransferase , cholesteryl ester , acyl coa , acyltransferases , cholesterol , chemistry , biochemistry , cholesterylester transfer protein , reverse cholesterol transport , coenzyme a , lipoprotein , endocrinology , enzyme , biology , biosynthesis , reductase
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. Edited by
Ming‐Hua XU