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Review
. 2015 Sep;242(1):29-36.
doi: 10.1016/j.atherosclerosis.2015.06.042. Epub 2015 Jul 2.

Liver X receptors at the intersection of lipid metabolism and atherogenesis

Stephen D Lee  1 , Peter Tontonoz  2
Affiliations
Review

Liver X receptors at the intersection of lipid metabolism and atherogenesis

Stephen D Lee et al. Atherosclerosis. 2015 Sep.
No abstract available

Keywords: Atherosclerosis; LXR; Lipid metabolism; Nuclear receptor.

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Figures

Figure 1
Figure 1
LXRs exert distinct effects on cholesterol and lipid metabolism in discrete cell types. Globally, LXR activation induces reverse cholesterol transport and reduces atherosclerotic plaque burden. Macrophage LXRs respond to oxidized sterol by increasing cholesterol efflux to lipoprotein acceptors, while decreasing uptake through the targeted degradation of the LDL receptor. In hepatocytes, LXRs increase the removal of cholesterol either by conversion to bile acids or direct secretion into the bile by ABC transporters. LXRs also induce a lipogenic program in hepatocytes, leading to increased triglyceride production and secretion. LXR activation in the small intestine decreases cholesterol absorption by increasing the expression of apical efflux transporters. Intestinal LXRs raise circulating HDL levels by inducing the expression of ABCA1. Portions of this figure were modified with permission from Macmillan Publishers Ltd: Nature Reviews Molecular Cell Biology (reference ).
Figure 2
Figure 2
Activation of LXRs is protective at different stages of atherosclerosis. In early lesions, cholesterol accumulates in macrophages, which adopt “foam cell” morphology. LXR activation in these cells reduces inflammation and improves cholesterol efflux. As atherosclerosis progresses the lesions become more complex, characterized by acellular lipid accumulation, a necrotic core, and thinning fibrous cap. In advanced lesions LXR activation induces the expression of genes that increase cholesterol efflux, reduce inflammation, stabilize the fibrous cap, induce macrophage egress from the lesion, repress apoptosis, and improve the clearance of apoptotic debris.-, -, -, , -, , -
See this image and copyright information in PMC

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