ApoE knock-out and knock-in mice: atherosclerosis, metabolic syndrome and beyond

Avani A. Pendse, Jose M. Arbones-Mainar, Lance A. Johnson, Michael Altenburg, and Nobuyo Maeda

Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7525

Corresponding Author: pendse{at}email.unc.edu

Given the multiple differences between mice and men, it was once thought that mice could not be used to model atherosclerosis, principally a human disease. Apolipoprotein E deficient (apoEKO) mice have convincingly changed this view, and the ability to model human-like plaques in these mice has provided scientists a platform to study multiple facets of atherogenesis and to explore potential therapeutic interventions. In addition to its well-established role in lipoprotein metabolism, recent observations of reduced adiposity and improved glucose homeostasis in apoEKO mice suggest that apoE may also play a key role in energy metabolism in peripheral organs including adipose tissue. Finally, along with apoEKO mice, knock-in mice expressing human apoE-isoforms in place of endogenous mouse apoE have provided insights into how quantitative and qualitative genetic alterations interact with the environment in the pathogenesis of complex human diseases.

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