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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2000;20:2503.)
© 2000 American Heart Association, Inc.

Editorial

Mouse Model of Unstable Atherosclerotic Plaque?

Godfrey S. Getz

From the Department of Pathology, University of Chicago, Chicago, Ill.

Correspondence to Dr Godfrey S. Getz, Department of Pathology, University of Chicago, 5841 S Mayfield Ave, BH-329, MC 3083, Chicago, IL 60637-1470. E-mail g-getz@uchicago.edu

Key Words: Editorials • apolipoprotein E • mouse • innominate artery • atherosclerosis • plaque complications

The study reported in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology by Rosenfeld et al¹ is very important in experimental atherosclerosis for 2 reasons. First, the study shows that there is an available murine model that expresses many features of the human plaque that are very relevant to the pathogenesis of clinically significant disease. Second, the study shows that there is a site of the arterial tree other than the aortic root that (in the appropriate models) almost invariably develops a lesion that begins with the accumulation of foam cells and progresses to the advanced lesion of the sort shown in the study. Many recent studies of atherosclerosis report on results exclusively based on the aortic root, not a frequent site of clinically significant lesions in humans. The innominate artery is an alternate site for the study of the pathogenesis of atherosclerosis. There has been shown to be a high frequency of extensive lesions at this site in apolipoprotein E (apoE)–null mice by 24 to 28 weeks of age, even if these mice are maintained on a chow diet (Reardon et al, unpublished observations, 2000), and this could be shortened if the mice are fed a Western-type diet. This makes it a site worthy of study even for shorter-term experiments. Although the aortic root may be easy to study, its lesion responses are not invariably reflective of the situation elsewhere in the vascular tree. We note that the aortic root and the innominate artery respond differently to immune deficiency . . . [Full Text of this Article]

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