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J Am Coll Cardiol, 2002; 39:1429-1435 © 2002 by the American College of Cardiology Foundation |
* Division of Cardiovascular Medicine, Department of Internal Medicine, University of Arkansas for Medical Sciences and the Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, USA
Manuscript received September 10, 2001; revised manuscript received February 7, 2002, accepted February 14, 2002.
* Reprint requests and correspondence: Dr. Jawahar L. Mehta, Division of Cardiovascular Medicine, University of Arkansas for Medical Sciences, 4301 West Markham Street, Slot 532, Little Rock, Arkansas 72205, USA.
mehtajl{at}uams.edu
Oxidatively modified low-density lipoprotein (ox-LDL) leads to endothelial activation, dysfunction and injury. Recently, a novel lectin-like receptor for ox-LDL (LOX-1) has been identified, primarily in the endothelial cells, and it allows uptake of ox-LDL into endothelial cells. This receptor is transcriptionally upregulated by tumor necrosis factor-alpha, angiotensin II, shear stress and ox-LDL itself. The expression of this receptor activates a variety of intracellular processes that lead to expression of adhesion molecules and endothelial activation. This receptor is highly expressed in the blood vessels of animals and humans with hypertension, diabetes mellitus and atherosclerosis. Expression of this receptor may also be relevant in intra-arterial thrombogenesis and myocardial ischemia-reperfusion injury. Identification and regulation of this receptor and understanding of signal transduction pathways may lead to new therapies of diseases characterized by endothelial dysfunction.
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