Liver X receptors as integrators of metabolic and inflammatory signaling
J. Clin. Invest. Noam Zelcer, et al. 116:607 doi:10.1172/JCI27883 [Go to this article.]

Figure 2
Role of LXRs in reverse cholesterol transport from macrophages. The uptake of modified lipoproteins by macrophages results in increased LXR transcriptional activity and efflux of cholesterol to lipid-poor apoA-I by ABCA1 and to HDL by ABCG1. In humans, but not mice, induction of CETP expression transfers lipid from HDL to LDL. Once HDL/LDL is taken up by the liver, LXR promotes net cholesterol excretion. In rodents, but not humans, LXR induces expression of Cyp7a1, which initiates the conversion of cholesterol into bile acids. LXRs also induce cholesterol secretion into bile through the transporters ABCG5 and ABCG8. In the intestine, apical ABCG5 and ABCG8 also act to limit dietary cholesterol uptake.