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(Circulation. 2005;111:3349-3351.)
© 2005 American Heart Association, Inc.

Editorial

Interplay Between Apolipoprotein E and Scavenger Receptor Class B Type I Controls Coronary Atherosclerosis and Lifespan in the Mouse

Sergio Fazio, MD, PhD; MacRae F. Linton, MD

From the Department of Medicine, Division of Cardiovascular Medicine (S.F., M.F.L.), the Department of Pathology (S.F.), and the Department of Pharmacology (M.F.L.), Vanderbilt University Medical Center, Nashville, Tenn.

Correspondence to Sergio Fazio, MD, PhD, Vanderbilt University Medical Center, Division of Cardiovascular Medicine, Room 383 PRB, Nashville, TN 37232–6300. E-mail sergio.fazio@vanderbilt.edu

Key Words: Editorials • apolipoproteins • arteriosclerosis

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

The mouse has become a standard model for the study of atherosclerosis induced by extreme dyslipidemia in genetically modified strains such as the apolipoprotein E (apoE)–deficient or the LDL-receptor–deficient mouse. Although the process of plaque formation appears to repeat the fundamental steps of the human disease, it has been notoriously difficult to reproduce in the mouse the clinical consequences of atherosclerosis, such as myocardial infarction and stroke, that so commonly in patients signal plaque rupture or total lumen occlusion.¹ The apoE-deficient mouse is a particularly interesting model because of its susceptibility to atherosclerotic lesions spanning from the aortic sinus to the abdominal aorta and involving the brachiocephalic and carotid arteries as well.^2,3 It has recently been reported that the brachiocephalic plaque in the apoE-deficient mouse is prone to rupture on feeding a high-fat diet for periods as short as 8 weeks,⁴ but even in this setting of exaggerated hypercholesterolemia, the aortic sinus and coronary tree do not appear to be susceptible to plaque rupture. Scavenger receptor class B type I (SR-BI) is a scavenger-type receptor expressed by many tissues and accepted by consensus to represent the docking receptor for HDL in the liver. SR-BI-deficient mice have raised HDL levels and increased atherosclerosis susceptibility on fat feeding.⁵ ApoE and SR-BI are both expressed, among other cells, by the hepatocyte and the macrophage. ApoE is an efficient ligand for receptor-mediated lipoprotein removal by the liver, but it is also a strong acceptor of cellular cholesterol. As such, it may control the rate . . . [Full Text of this Article]

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