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(Hypertension. 2007;50:276.)
© 2007 American Heart Association, Inc.

Brief Reviews

Effects of Native and Modified Low-Density Lipoproteins on Monocyte Recruitment in Atherosclerosis

From the Departments of Biomedical Engineering (C.A.G., K.L.), Pharmacology (N.L.), Molecular Physiology and Biological Physics (K.L.), and the Robert M. Berne Cardiovascular Research Center (C.A.G., N.L., K.L.), University of Virginia, Charlottesville.

Correspondence to Klaus Ley, MD, Robert M. Berne Cardiovascular Research Center, University of Virginia, P.O. Box 801394, Charlottesville, VA 22908. E-mail klausley@virginia.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Atherosclerosis is a chronic inflammatory disease of the arterial wall^1–3 with enormous epidemiological relevance.^4,5 Recruitment of monocytes to the vascular wall is a key feature in the pathogeneses of atherosclerotic lesions. Through a complex cascade of interactions between adhesion molecules and chemotactic factors, monocytes enter the subendothelial space, where they develop into macrophages, foam cells, and dendritic cells under the influence of cytokines, growth factors, and lipoproteins.^6–8 Foam cells eventually undergo secondary necrosis and form the lipid core of advanced atherosclerotic plaques. When exposed by rupture or erosion, it triggers acute thrombotic events leading to myocardial infarction and strokes.⁹

Elevated serum levels of low-density lipoprotein (LDL) (see the Table for abbreviations) are a major risk factor for the development of atherosclerosis.⁴ Apart from epidemiological evidence for the proatherogenic role of lipoproteins, mechanistic studies suggest that they play a role in monocyte recruitment to the vessel wall and the progression of macrophages to foam cells. LDL does not only occur in its native form, but modified forms of LDL—eg, by oxidation, aggregation, or other processes—are thought to be even more proatherogenic.^10–13

Even though numerous reviews have focused on monocyte recruitment to the arterial wall^14–16 or on effects of LDL on foam cell formation^7,14 in atherogenesis, no recent review has specifically addressed the effects of native and modified LDL on monocyte recruitment to the vessel wall. Here, we discuss the molecular effects of LDL on monocyte recruitment to the arterial wall as a crucial step in the . . . [Full Text of this Article]

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