期刊
JOURNAL OF LIPID RESEARCH
卷 50, 期 -, 页码 S80-S85出版社
ELSEVIER
DOI: 10.1194/jlr.R800044-JLR200
关键词
ABCA1; ABCG1; ABCG4; ABCG5/8; cholesterol
资金
- National Institutes of Health [NIH30568, NIH68445]
- Laubisch Fund
- Pfizer, Inc.
Mammalian cells have developed various responses to minimize accumulation of unesterified cholesterol, as the latter can result in cell toxicity and death [reviewed in this edition by Bjorkhem (Bjorkhem, I. 2009. Are side-chain oxidized oxysterols regulators also in vivo? J. Lipid Res. In press)]. These responses include esterification to sequester excess sterol in intracellular lipid droplets, repression of both cholesterol synthesis and LDL receptor expression (thus reducing endocytosis of LDL), and induction of a panoply of genes that promote sterol efflux and affect lipid metabolism. The nuclear receptor liver-X-receptor (LXR) functions as a cellular sterol sensor and plays a critical role in these latter transcriptional changes [reviewed in this edition by Glass (Shibata, N., and Glass C, K. 2009. Regulation of macrophage function in inflammation and atherosclerosis. J. Lipid Res. In press)]. Activation of LXR by either endogenous oxysterols or synthetic agonists induces the expression of many genes, including those encoding ATP-binding cassette (ABC) transporters ABCA1, ABCG1, ABCG5, and ABCG8.jlr As discussed below, these four proteins function to promote sterol efflux from cells.-Baldan, A., D. D. Bojanic, and P. A. Edwards. The ABCs of sterol transport. J. Lipid Res. 2009. S80-S85.
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