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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:2209.)
© 2004 American Heart Association, Inc.

Editorials

24(S),25-Epoxycholesterol—A Potential Friend

Ingemar Bjorkhem; Ulf Diczfalusy

From the Division of Clinical Chemistry, Department of Laboratory Medicine, Karolinska University Hospital, Huddinge, Sweden

Correspondence to Ingemar Bjorkhem, Division of Clinical Chemistry, C1 62, Department of Laboratory Medicine, Karolinska University Hospital, Stockholm, Hu S-141 86, Sweden. E-mail ingemar.bjorkhem@kus.se

An extract of the first 250 words of the full text is provided, because this article has no abstract.

According to current concepts, oxysterols are the physiological mediators of a number of cholesterol-induced metabolic effects (for a review, see Bjorkhem et al¹). Most of the evidence for this is however still indirect, and there is a discrepancy between the great number of studies demonstrating potent effects of oxysterols under in vitro conditions and the few studies consistent with a regulatory effect in vivo. Oxysterol binding proteins and receptors are doubtless of regulatory importance in cholesterol turnover, but the physiological ligand(s) to the proteins have not yet been defined with certainty. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, the article by Wong et al² gives strong support for the contention that the oxysterol 24(S),25-epoxycholesterol, an efficient activator of the nuclear receptor LXR in vitro, is an important mediator of statin-induced effects on cholesterol homeostasis in THP-1 macrophages.

See page 2365

The first important message of the article is that a statin appears to have a negative effect on cholesterol efflux both from the human macrophage cell line THP-1 and from primary human macrophages, most probably because of a documented reduced expression of the cholesterol transporters ABCA1, ABCG1, and the nuclear receptor LXR. The finding is in accordance with several previous reports demonstrating that statins may reduce the constitutive activity of LXR and LXR-activated genes (see Wong et al² and references therein). The authors of the present article point out that reduced cholesterol efflux would be predicted to be proatherogenic, in marked contrast to all the . . . [Full Text of this Article]

Related Article:

Statins Inhibit Synthesis of an Oxysterol Ligand for the Liver X Receptor in Human Macrophages With Consequences for Cholesterol Flux

Jenny Wong, Carmel M. Quinn, and Andrew J. Brown
Arterioscler Thromb Vasc Biol 2004 24: 2365-2371. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				J. Wong, C. M. Quinn, I. C. Gelissen, and A. J. Brown Endogenous 24(S),25-Epoxycholesterol Fine-tunes Acute Control of Cellular Cholesterol Homeostasis J. Biol. Chem., January 11, 2008; 283(2): 700 - 707. [Abstract] [Full Text] [PDF]