title: Mouse models of experimental atherosclerosis.
abstract: Since 1992 the mouse has become an excellent model for experimental atherosclerosis research. Until 1992, the diet -- induced atherosclerosis mouse model has been used effectively, but the lesions tended to be small and were limited to early fatty-streak stage. This model was also criticized because of the toxicity and inflammatory responses due to the diet. In 1992 the first line of gene targeted animal models, namely apolipoprotein E -- knockout mice was developed. Of the genetically engineered models, the apoE -- deficient model is the only one that develops extensive atherosclerotic lesions on a chow diet. It is also the model in which the lesions have been characterized most thoroughly. The lesions develop into fibrous plaques; however, there is no evidence that plaque rupture occurs in this model. The LDL receptor - deficient model has elevated LDL levels, but no lesions, or only very small lesions, form on the chow diet, however, robust lesions do form on the western-type diet. The creation of apoE -- knockout mice has changed the face of atherosclerosis research.
authors.affiliation: Department of Pharmacology, Jagiellonian University School of Medicine, Krakow, Poland.
authors.forename: J
authors.initials: J
authors.lastname: Jawień
authors.forename: P
authors.initials: P
authors.lastname: Nastałek
authors.forename: R
authors.initials: R
authors.lastname: Korbut
mesh_terms: D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency / Q000235:genetics*; D001161:Arteriosclerosis / Q000097:blood / Q000235:genetics* / Q000378:metabolism; D004036:Diet, Atherogenic; D004195:Disease Models, Animal; D018390:Gene Targeting; D051379:Mice; D018345:Mice, Knockout; D011973:Receptors, LDL / Q000172:deficiency / Q000235:genetics*
chemical_list: D001057:Apolipoproteins E; D011973:Receptors, LDL