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Liver X Receptors, Atherosclerosis and Inflammation

Authors
  • Michael, Daryn R.1
  • Ashlin, Tim G.1
  • Buckley, Melanie L.1
  • Ramji, Dipak P.1
  • 1 Cardiff University, Cardiff School of Biosciences, Museum Avenue, Cardiff, CF10 3AX, UK , Cardiff (United Kingdom)
Type
Published Article
Journal
Current Atherosclerosis Reports
Publisher
Springer-Verlag
Publication Date
Mar 15, 2012
Volume
14
Issue
3
Pages
284–293
Identifiers
DOI: 10.1007/s11883-012-0239-y
Source
Springer Nature
Keywords
License
Yellow

Abstract

Liver X receptors (LXRs) belong to the nuclear receptor superfamily of ligand-dependent transcription factors. LXRs are activated by oxysterols, metabolites of cholesterol, and therefore act as intracellular sensors of this lipid. There are two LXR genes (α and β) that display distinct tissue/cell expression profiles. LXRs interact with regulatory sequences in target genes as heterodimers with retinoid X receptor. Such direct targets of LXR actions include important genes implicated in the control of lipid homeostasis, particularly reverse cholesterol transport. In addition, LXRs attenuate the transcription of genes associated with the inflammatory response indirectly by transrepression. In this review, we describe recent evidence that both highlights the key roles of LXRs in atherosclerosis and inflammation and provides novel insights into the mechanisms underlying their actions. In addition, we discuss the major limitations of LXRs as therapeutic targets for the treatment of atherosclerosis and how these are being addressed.

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