upture 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 Thsen et al 1 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).
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Mark W. Majesky (2002) studied this question.