载脂蛋白B
转基因小鼠
发病机制
突变体
生物
载脂蛋白E
脂蛋白
转基因
病变
低密度脂蛋白受体
受体
胆固醇
疾病
内分泌学
内科学
基因
免疫学
医学
遗传学
病理
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:1996-05-03
卷期号:272 (5262): 685-688
被引量:701
标识
DOI:10.1126/science.272.5262.685
摘要
As a species the mouse is highly resistant to atherosclerosis. However, through induced mutations it has been possible to develop lines of mice that are susceptible to this disease. For example, mice that are deficient in apolipoprotein E, a ligand important in lipoprotein clearance, develop atherosclerotic lesions resembling those observed in humans. These lesions are exacerbated when the mice are fed a high-cholesterol, high-fat, Western-type diet. Other promising models are mice that are deficient in the low density lipoprotein receptor and transgenic mice that express human apolipoprotein B and transdominant mutant forms of apolipoprotein E. These models are now being used to study the pathogenesis of atherosclerotic lesions, as well as the influence of genetics, environment, hormones, and drugs on lesion development.
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