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Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E.
Apolipoprotein E (apoE) is a ligand for receptors that clear remnants of chylomicrons and very low density lipoproteins. Lack of apoE is, therefore, expected to cause accumulation in plasma of cholesterol-rich remnants whose prolonged circulation should be atherogenic. ApoE-deficient mice generated by gene targeting were used to test this hypothesis and to make a mouse model for spontaneous atherosclerosis. The mutant mice had five times normal plasma cholesterol, and developed foam cell-rich depositions in their proximal aortas by age 3 months. These spontaneous lesions progressed and caused severe occlusion of the coronary artery ostium by 8 months. The severe yet viable phenotype of the mutants should make them valuable for investigating genetic and environmental factors that modify the atherogenic process.[1]References
- Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E. Zhang, S.H., Reddick, R.L., Piedrahita, J.A., Maeda, N. Science (1992) [Pubmed]
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