This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Daugherty, A. Articles by Lu, H. Search for Related Content PubMed PubMed Citation Articles by Daugherty, A. Articles by Lu, H. Related Collections Related Article

(Circulation Research. 2008;102:1445.)
© 2008 American Heart Association, Inc.

Editorials

As Macrophages Indulge, Atherosclerotic Lesions Bulge

Alan Daugherty, Debra L. Rateri, Hong Lu

From the Cardiovascular Research Center, University of Kentucky, Lexington.

Correspondence to Alan Daugherty, Wethington Building, Room 521, University of Kentucky, Lexington, KY 40536-0200. E-mail Alan. Daugherty@uky.edu

See related article, pages 1492–1501

Key Words: macrophages • atherosclerosis • lipid deposition

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

Lipid-laden macrophages are the predominant cell type in the formative stages of atherosclerosis in most animal models and humans.^1–3 Lipid deposition appears as large numbers of intracellular droplets that have a foam-like appearance when paraffin-embedded tissue sections are viewed at high magnification. Consequently, the descriptive name of foam cells is applied to these lipid-laden macrophages. Originating from recruited monocytes, it has been hypothesized that foam cells remove lipoproteins that have been retained and modified in the subendothelial space.⁴ For this function to be beneficial, lipid-laden macrophages would subsequently egress from the area of the forming lesion. However, the system frequently goes awry. Macrophages recruited to the arterial wall become grossly engorged with lipid, presumably because of an imbalance in lipid metabolism. In this greatly hypertrophied state, macrophages are unable to transit through the endothelium and be transferred back to the blood compartment. Therefore, instead of exiting the artery, these cells are retained and accumulate. In addition to these cells forming the mass of the evolving lesions, there is also the potential for secretion of many bioactive molecules that may perpetuate and modify the atherogenic process.

There have been many approaches to modify the development of foam cells by manipulating intracellular transport, intracellular storage, or efflux of lipids. The transport of extracellular lipid to form intracellular droplets is presumed to occur via endocytosis through lipoprotein receptors that are not downregulated by increased cholesterol content. There are many classes of scavenger receptors that transport modified lipoproteins into macrophages, of which the most . . . [Full Text of this Article]

Related Article:

Deficiency of Adipose Differentiation-Related Protein Impairs Foam Cell Formation and Protects Against Atherosclerosis

Antoni Paul, Benny Hung-Junn Chang, Lan Li, Vijay K. Yechoor, and Lawrence Chan
Circ. Res. 2008 102: 1492-1501. [Abstract] [Full Text] [PDF]