Breslow J L
Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York, 10021, USA.
Science. 1996 May 3;272(5262):685-8. doi: 10.1126/science.272.5262.685.
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.
作为一个物种，小鼠对动脉粥样硬化具有高度抗性。然而，通过诱导突变，已经能够培育出易患这种疾病的小鼠品系。例如，载脂蛋白E缺乏的小鼠，载脂蛋白E是脂蛋白清除中重要的配体，会出现类似于人类中观察到的动脉粥样硬化病变。当给这些小鼠喂食高胆固醇、高脂肪的西式饮食时，这些病变会加剧。其他有前景的模型是低密度脂蛋白受体缺乏的小鼠以及表达人类载脂蛋白B和载脂蛋白E的显性突变形式的转基因小鼠。这些模型现在正被用于研究动脉粥样硬化病变的发病机制，以及遗传、环境、激素和药物对病变发展的影响。
