Spontaneous Hypercholesterolemia and Arterial Lesions in Mice Lacking Apolipoprotein E

DOI Web Site 被引用文献82件
  • Sunny H. Zhang
    Department of Pathology, University of North Carolina, Chapel Hill, NC 27599-7525.
  • Robert L. Reddick
    Department of Pathology, University of North Carolina, Chapel Hill, NC 27599-7525.
  • Jorge A. Piedrahita
    Department of Veterinary Anatomy and Public Health, Texas A&M University, College Station, TX 77840-4458.
  • Nobuyo Maeda
    Department of Pathology, University of North Carolina, Chapel Hill, NC 27599-7525.

抄録

<jats:p>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.</jats:p>

収録刊行物

  • Science

    Science 258 (5081), 468-471, 1992-10-16

    American Association for the Advancement of Science (AAAS)

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