on April 15, 2004
Arteriosclerosis, Thrombosis, and Vascular Biology. 2004
Published online before print April 15, 2004, doi: 10.1161/01.ATV.0000128849.12617.f4
Published online before print April 15, 2004, doi: 10.1161/01.ATV.0000128849.12617.f4
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Submitted on December 29, 2003
Accepted on April 6, 2004
Atherosclerosis in the Apolipoprotein E-Deficient Mouse: A Decade of Progress
Karen S. Meir and Eran Leitersdorf *
From the Department of Pathology (K.S.M.), the Center for Research, Prevention, and Treatment of Atherosclerosis (K.S.M., E.L.), and the Department of Internal Medicine B (E.L.), Hadassah University Hospital, Jerusalem, Israel.
* To whom correspondence should be addressed. E-mail: eranL{at}hadassah.org.il.
Abstract--Arguably the most critical advancement in the elucidation of factors affecting atherogenesis has been the development of mouse models of atherosclerosis. Among available models, the apolipoprotein E-deficient (apoE-/-) mouse is particularly popular because of its propensity to spontaneously develop atherosclerotic lesions on a standard chow diet. A Medline search reveals over 645 articles dedicated to studies using this reliable and convenient "super" animal model since its inception1,2 with a more or less steady increase from year to year. This review will examine our present understanding of the pathology and progression of plaques in this animal and highlight some of the nutritional, pharmacological, and genetic studies that have enhanced this understanding.
Key words: apolipoprotein E • atherosclerosis • knockout • mouse model
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