ABSTRACT
The use of the mouse as a model to study atherosclerosis has lagged behind its use to study a variety of other human conditions. This relates to the relative resistance of mice to develop atherosclerosis and the availability of other mammals such as rabbits and pigs that are significantly more susceptible to atherosclerosis. This chapter outlines some of the research using transgenic mice to assess the impact of various genes involved in lipid transport on atherosclerosis susceptibility. Familial hypercholesterolemia is a common cause of markedly increased atherosclerosis susceptibility in humans. This condition is the result of an absence or an abnormal function of the low density lipoprotein (LDL) receptor. Generation of transgenic mice overexpressing apolipoprotein B (apoB), the primary protein component of both LDL and very low density lipoproteins, has been hindered by the extremely large size of the apoB protein and genomic size.
