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Myeloperoxidase-Mediated Dysfunctional High-Density Lipoprotein
Author(s) -
Godfrey S. Getz,
Catherine A. Reardon
Publication year - 2014
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.114.303282
Subject(s) - dysfunctional family , myeloperoxidase , high density lipoprotein , chemistry , medicine , inflammation , clinical psychology , cholesterol
The oxidation of lipoproteins plays an important role in atherogenesis. Most studies have focused on the oxidation of low-density lipoprotein, occurring to a significant extent in the arterial intima leading to the formation of the characteristic foam cell of the atherosclerotic plaque.1 However, the oxidation of the proteins of high-density lipoprotein (HDL) is thought to substantially attenuate the atheroprotective effects of this lipoprotein. Among the agents that potentially play an important role in oxidizing HDL is myeloperoxidase, an enzyme found in neutrophils, monocytes, and subsets of macrophages. Myeloperoxidase levels in the blood and blood leukocytes have been reported to be elevated in patients with coronary artery disease.2 Its level may be a valuable risk factor able to predict a major cardiac event in patients with chest pain.3See accompanying article on page 779Apolipoprotein A-I (apoA-1) is thought to have several atheroprotective influences.4 In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology , Hewing et al …

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