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Kristiaan Wouters, Ronit Shiri-Sverdlov, Patrick J. van Gorp, Marc van Bilsen, Marten H. Hofker

Understanding hyperlipidemia and atherosclerosis: lessons from genetically modified apoe and ldlr mice

Keywords: apolipoprotein E (ApoE), gene targeting, genetics, Genomics, hyperlipoproteinemia, low-density protein receptor (LDLR), transgenesis

Hyperlipidemia is the most important risk factor for atherosclerosis, which is the major cause of cardiovascular disease. The etiology of hyperlipidemia and atherosclerosis is complex and governed by multiple interacting genes. However, mutations in two genes have been shown to be directly involved, i.e., the low-density lipoprotein receptor (LDLR) and apolipoprotein E (ApoE). Genetically modified mouse models have been instrumental in elucidating the underlying molecular mechanisms in lipid metabolism. In this review, we focus on the use of two of the most widely used mouse models, ApoE- and LDLR-deficient mice. After almost a decade of applications, it is clear that each model has unique strengths and drawbacks when carrying out studies of the role of additional genes and environmental factors such as nutrition and lipid-lowering drugs. Importantly, we elaborate on mice expressing mutant forms of APOE, including the APOE3Leiden ( APOE3L) and the APOE2 knock-in ( APOE2k) mouse models. These models have outstanding potential, as they are highly responsive to dietary factors and pharmacological interventions.

Clinical Chemical Laboratory Medicine, Walter de Gruyter

Print ISSN: 1434-6621
Volume: 43, 05/2005
Pages: 470 - 479

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