BIOMEDICINE: A Heart Attack Mouse

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Science  18 Jan 2002:
Vol. 295, Issue 5554, pp. 407a
DOI: 10.1126/science.295.5554.407a

In the United States alone, nearly one million people die each year from heart disease. Elevated serum cholesterol is a well-established risk factor for coronary artery atherosclerosis, a leading cause of myocardial infarctions (heart attacks). However, the precise role that lipoprotein metabolism defects and atherosclerosis play in the pathogenesis of myocardial infarction remains poorly understood, in part because of the limited availability of small animal models that combine these cardinal features of human cardiovascular disease.

New work by Braun et al. indicates that mice doubly deficient in apolipoprotein E (apoE) and the high-density lipoprotein receptor SR-BI may provide such a model. When fed a normal chow diet, these mice exhibited high cholesterol levels, accelerated atherosclerosis, and occlusive lesions in the coronary artery that were remarkably similar to those seen in humans with heart disease. Importantly, the mice spontaneously developed myocardial infarctions and cardiac dysfunction that contributed to their death at a very young age (6 to 8 weeks). In addition to providing new insight into the pathogenesis of heart attacks, these mice may prove to be valuable tools for the testing of new therapies for cardiovascular disease. — PAK

Circulation Res.

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