Mouse models of hyperlipidemia and atherosclerosis.
The mouse is the most utilized model to study lipids and atherosclerosis. Before the advent of the techniques of genetic manipulation it was well known that different inbred strains had varying degrees of susceptibility to diet-induced atherosclerosis. The C57BL/6 mouse was adopted as the standard even though the arterial lesions induced by even extreme diets were limited in size, complexity, and distribution. This changed with the production of several gene knockout and transgenic mice, which in many cases produced remarkable effects on plasma lipoproteins and arterial lesions even without dietary manipulations. The most typical example remains the apoE deficient model, in which a massive hyperlipidemia is accompanied with the development of severe atherosclerotic plaques at the aortic root and throughout the aortic tree. With the creation of the LDL receptor knockout, and the different knockout and transgenic mice with changes in apoB, apoE, and the HDL system, a solid body of new information has emerged on the mechanisms regulating plasma lipoprotein levels and controlling the initial stages of atherogenesis. This paper presents an overview of the most utilized mouse models and a summary of the results obtained with the technique of bone marrow transplantation, an approach to study macrophages in atherosclerosis.
Vanderbilt University School of Medicine, Division of Cardiovascular Medicine, Department of Medicine, 315 Medical Research Building II, Nashville, TN 37232, USA. sergio.fazio@mcmail.vanderbilt.edu
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D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency / Q000235:genetics; D001161:Arteriosclerosis / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D006949:Hyperlipidemias / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D011973:Receptors, LDL / Q000172:deficiency / Q000235:genetics
D001057:Apolipoproteins E; D011973:Receptors, LDL