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(Circulation. 2002;105:2010.)
© 2002 American Heart Association, Inc.

Editorial

Mouse Model for Atherosclerotic Plaque Rupture

Mark W. Majesky, PhD

From the Departments of Pathology and Molecular and Cellular Biology, Baylor College of Medicine, Houston, Tex.

Correspondence to Mark W. Majesky, PhD, Department of Pathology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030. E-mail mmajesky@bcm.tmc.edu

Key Words: Editorials • fibrin • apoptosis • apolipoproteins • plaque

Rupture of advanced human atherosclerotic plaques can precipitate coronary thrombosis, myocardial infarction, and sudden death, but insights into the causes and treatment of plaque rupture have been hampered by lack of a suitable animal model. Particularly desirable would be a model of plaque rupture that would take advantage of current and forthcoming mouse mutant alleles. It is therefore of considerable interest that the study by von der Thüsen et al¹ in this issue of Circulation reports the characterization of a model of induced plaque rupture in apolipoprotein E–deficient (ApoE^-/-) mice secondary to cap thinning produced by overexpression of p53, a proapoptotic stimulus for plaque smooth muscle cells (SMCs).

See p 2064

Vulnerable Atherosclerotic Plaques

Erosion, ulceration, or rupture of the surface of atherosclerotic plaques exposes highly thrombogenic components in the interior of the lesion. SMC apoptosis, loss of extracellular matrix (ECM) integrity, and inflammatory cell accumulation in the fibrous cap are thought to be important pathogenic factors leading to plaque instability.² Previous attempts to produce an animal model for plaque rupture have proved to be less than optimal. The ability to carry out genetic analyses in mice, together with existing mouse models for atherosclerosis, proves that a mouse model of plaque rupture would be extremely valuable. Unfortunately, atherosclerotic plaques in mice generally are regarded as resistant to plaque rupture. Johnson and Jackson³ reported that ApoE^-/- mice fed a high-fat diet for 1 year exhibited occlusive thrombus formation in the brachiocephalic artery. Histological examination of these vessels showed thin caps, loss of plaque . . . [Full Text of this Article]

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