Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/65862
Citations
Scopus Web of Science® Altmetric
?
?
Type: Journal article
Title: Hydroxyoctadecadienoic acids: novel regulators of macrophage differentiation and atherogenesis
Author: Vangaveti, V.
Baune, B.
Kennedy, R.
Citation: Therepeutic Advances in Endocrinology and Metabolic Disorders, 2010; 1(2):51-60
Publisher: Sage Publications Ltd
Issue Date: 2010
ISSN: 2042-0188
2042-0196
Statement of
Responsibility: 
Venkat Vangaveti, Bernhard T. Baune and R. Lee Kennedy
Abstract: Hydroxyoctadecadienoic acids (HODEs) are stable oxidation products of linoleic acid, the generation of which is increased where oxidative stress is increased, such as in diabetes. In early atherosclerosis, 13-HODE is generated in macrophages by 15-lipoxygenase-1. This enhances protective mechanisms through peroxisome proliferator-activated receptor (PPAR)-γ activation leading to increased clearance of lipid and lipid-laden cells from the arterial wall. In later atherosclerosis, both 9-HODE and 13-HODE are generated nonenzymatically. At this stage, early protective mechanisms are overwhelmed and pro-inflammatory effects of 9-HODE, acting through the receptor GPR132, and increased apoptosis predominate leading to a fragile, acellular plaque. Increased HODE levels thus contribute to atherosclerosis progression and the risk of clinical events such as myocardial infarction or stroke. Better understanding of the role of HODEs may lead to new pharmacologic approaches to modulate their production or action, and therefore lessen the burden of atherosclerotic disease in high-risk patients.
Keywords: atherosclerosis; diabetes; oxidative stress; oxidized lipids; G protein-coupled receptors
Rights: © The Author(s), 2010
RMID: 0020111230
DOI: 10.1177/2042018810375656
Appears in Collections:Psychiatry publications

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.