Lipid oxidation by hypochlorous acid: chlorinated lipids in atherosclerosis and myocardial ischemia

被引:67
作者
Ford, David A. [1 ]
机构
[1] St Louis Univ, Sch Med, Cardiovasc Res Ctr, Dept Biochem & Mol Biol, St Louis, MO 63104 USA
关键词
atherosclerosis; fatty acid; fatty aldehyde; lipid monocyte; myeloperoxidase; myocardial ischemia; neutrophil; plasmalogen; LOW-DENSITY-LIPOPROTEIN; APOLIPOPROTEIN-A-I; VINYL ETHER BOND; ABCA1-DEPENDENT CHOLESTEROL TRANSPORT; MYELOPEROXIDASE-CATALYZED OXIDATION; CARDIAC SARCOPLASMIC-RETICULUM; PLATELET-ACTIVATING-FACTOR; PEROXIDE-CHLORIDE SYSTEM; ACUTE CORONARY SYNDROMES; SCAVENGER RECEPTOR CD36;
D O I
10.2217/CLP.10.68
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
Leukocytes, containing myeloperoxidase (MPO), produce the reactive chlorinating species, HOCl and they have important roles in the pathophysiology of cardiovascular disease. Leukocyte-derived HOCl can target primary amines, alkenes and vinyl ethers of lipids, resulting in chlorinated products. Plasmalogens are vinyl ether-containing phospholipids that are abundant in tissues of the cardiovascular system. The HOCl oxidation products derived from plasmalogens are alpha-chlorofatty aldehyde and unsaturated molecular species of lysophosphatidylcholine; alpha-chlorofatty aldehyde is the precursor of both alpha-chlorofatty alcohol and alpha-chlorofatty acid. Both alpha-chlorofatty aldehyde and alpha-chlorofatty acid accumulate in activated neutrophils and have disparate chemotactic properties. In addition, alpha-chlorofatty aldehyde increases in activated monocytes, human atherosclerotic lesions and rat infarcted myocardium. This article addresses the pathways for the synthesis of these lipids and their biological targets.
引用
收藏
页码:835 / 852
页数:18
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