Abstract
Proteomic Analysis of Liver from Human Lipoprotein(a) Transgenic Mice Shows an Oxidative Stress and Lipid Export Response
Highlights
IntroductionThe two most widely used models are the apolipoprotein E deficient (ApoE-/-) mouse [1] with elevated levels of cholesterol and triglyceride due to defective remnant lipoprotein clearance [2] and the lowdensity lipoprotein receptor deficient (LDLR-/-) mouse with elevated cholesterol due to defective low-density lipoprotein (LDL) uptake
Mouse models of hypercholesterolaemia are widely used to study atherosclerosis
Compared to the apoE-/- and LDLR-/- mice, the Lp(a) mice are slow to develop atherosclerosis [5] but are relevant to the human situation due to the elevated levels of human low-density lipoprotein (LDL) and presence of Lp(a), both of which have been well established as important cardiovascular risk factors in humans [6, 7]
Summary
The two most widely used models are the apolipoprotein E deficient (ApoE-/-) mouse [1] with elevated levels of cholesterol and triglyceride due to defective remnant lipoprotein clearance [2] and the lowdensity lipoprotein receptor deficient (LDLR-/-) mouse with elevated cholesterol due to defective low-density lipoprotein (LDL) uptake. Both have served as a base for genetic, pharmacologic, and dietary interventions to establish the effects on atherosclerosis development [3]. The antioxidant response can be reproduced in human liver cells treated with Lp(a)
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