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Experimental Hypercholesterolemia in Genetic ApoE−/−/Lrp5−/− Mice: Proof of Principle

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Molecular Biology of Valvular Heart Disease
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Abstract

The low-density lipoprotein-related receptor 5 and 6 (Lrp5 and Lrp6) genes were cloned in 1998 based on their homology with the low-density lipoprotein receptor (LDLR) [1–4]. Mutations in either LRP5 or LRP6, proteins have caused a number of disease processed in the field of bone [5, 6], and have been associated with cardiovascular disease [4, 7–9]. The LDL-Density-Pressure theory [10] combines the structure, function analysis of these co-receptors with the results from the genetic studies to provide a unique hypothesis for the role of these receptors in the heart. This chapter provides the genetic mouse evidence to demonstrate that in the presence of experimental hypercholesterolemia, Lrp5/6 receptors, Runx2 genes are up-regulated in the presence of cholesterol and mediate calcification by MicroCT analysis.

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Correspondence to Nalini M. Rajamannan MD .

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Rajamannan, N.M. (2014). Experimental Hypercholesterolemia in Genetic ApoE−/−/Lrp5−/− Mice: Proof of Principle. In: Rajamannan, N. (eds) Molecular Biology of Valvular Heart Disease. Springer, London. https://doi.org/10.1007/978-1-4471-6350-3_8

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  • DOI: https://doi.org/10.1007/978-1-4471-6350-3_8

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