小鼠动脉粥样硬化的基因修饰因子。
Genetic modifiers of atherosclerosis in mice.
作者信息
Knowles J W, Maeda N
机构信息
Department of Pathology and Laboratory Medicine and the Curriculum in Genetics and Molecular Biology, University of North Carolina, Chapel Hill, NC, USA.
出版信息
Arterioscler Thromb Vasc Biol. 2000 Nov;20(11):2336-45. doi: 10.1161/01.atv.20.11.2336.
Abstract
Atherosclerosis is a complex, multifactorial disease with both genetic and environmental determinants. Experimental investigation of the effects of these determinants on the development and progression of atherosclerosis has been greatly facilitated by the use of targeted mouse models of the disease, particularly those resulting from the absence of functional genes for apolipoprotein E or the low density lipoprotein receptor (LDLR). This review focuses on the influence on atherosclerosis of combining apoE or LDLR deficiencies with factors affecting atherogenesis, including (1) inflammatory processes, (2) glucose metabolism, (3) blood pressure, and (4) coagulation and fibrinolysis. We also discuss the general problem of using the mouse to test the effects on atherogenesis of human polymorphic variations and future ways of enhancing the usefulness of these mouse models.
摘要
动脉粥样硬化是一种复杂的多因素疾病，具有遗传和环境决定因素。使用该疾病的靶向小鼠模型，特别是那些由于载脂蛋白E或低密度脂蛋白受体（LDLR）功能基因缺失而产生的模型，极大地促进了对这些决定因素对动脉粥样硬化发展和进展影响的实验研究。本综述重点关注apoE或LDLR缺陷与影响动脉粥样硬化形成的因素相结合对动脉粥样硬化的影响，这些因素包括：（1）炎症过程；（2）葡萄糖代谢；（3）血压；（4）凝血和纤维蛋白溶解。我们还讨论了使用小鼠来测试人类多态性变异对动脉粥样硬化形成影响的一般问题，以及提高这些小鼠模型实用性的未来方法。
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