Abstract
The Liver X Receptors (LXRα, NR1H3; LXRβ, NR1H2) encode highly homologous transcription factors that are members of the nuclear receptor superfamily of proteins. Both LXRα and LXRβ form heterodimers with the obligate partner 9- cis retinoic acid receptor α (RXRα; NR2B1). LXR/RXR heterodimers function as sensors for cellular oxysterols and, when activated by these agonists, increase the expression of genes that control sterol and fatty acid metabolism/homeostasis. These conclusions are based on studies that: (i) identified oxysterols as the natural ligands for both LXRα and LXRβ; (ii) identified target genes that are activated by LXR/RXR; (iii) generated mice that were deficient in LXRα, LXRβ or both LXRα and LXRβ; (iv) identified synthetic LXR ligands that were extremely potent in vivo; and (v) demonstrated significant alterations in cholesterol and fatty acid homeostasis in animals in which LXR had been either activated or deleted. These findings suggest that synthetic LXR ligands may prove useful in the treatment of certain dyslipidemias. In this review, we summarize the current status of this rapidly moving area with a special emphasis on the potential for pharmacological intervention.
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