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JCI table of contents -- July 26, 2007

ia, Los Angeles, show that activation of LXR-beta by a synthetic compound is able to reverse atherosclerosis and cholesterol overload in mice.

The authors began by studying mice lacking apolipoprotein E (apoE; a protein that functions in cholesterol distribution among cells), which have increased cholesterol levels and are predisposed to develop atherosclerosis. They showed that the loss of LXR-alpha in these animals results in a striking body-wide accumulation of cholesterol and accelerated atherosclerosis. This observation suggests that LXR-beta alone is unable to maintain homeostasis under conditions of cholesterol overload. Surprisingly, however, administration of a synthetic compound that activates LXR-beta, was able to compensate for the loss of LXR-alpha, reduce cholesterol overload and reduce atherosclerosis. The results of the study suggests that LXR-alpha has an essential role in maintaining cholesterol homeostasis in conditions of cholesterol overload such as hypercholesterolemia and lend support to the notion that future drug development studies should examine targeting LXR-beta.

TITLE: Ligand activation of LXR-beta reverses atherosclerosis and cellular cholesterol overload in mice lacking LXR-alpha and apoE

AUTHOR CONTACT:

Peter Tontonoz

University of California, Los Angeles, David Geffen School of Medicine, Los Angeles, California, USA.

Phone : (310) 206-4546; Fax: (310) 267-0382; E-mail: ptontonoz@mednet.ucla.edu

View the PDF of this article at: https://www.the-jci.org/article.php?id=31909


IMMUNOLOGY

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The protein known as SLAT (SWAP-70like adaptor of T cells) was recently identified, however its physiological function remained unclear. In a study appearing online o
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Contact: Brooke Grindlinger
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
26-Jul-2007


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