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Journal of Lipid Research, Vol. 50, S277-S281, April 2009
Regulation of macrophage function in inflammation and atherosclerosis
Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093-0651 This work was supported by the LIPID MAPS Large Scale Collaborative Grant number GM069338 from the National Institutes of Health (C.K.G.) and an American Heart Association Fellowship (N.S.). Published, JLR Papers in Press, November 5, 2008.
1 To whom correspondence should be addressed. e-mail: ckg{at}ucsd.edu
Atherosclerosis can be considered as both a chronic inflammatory disease and a lipid metabolism disorder. Innate immunity pathways have long been suspected to contribute to the initiation and progression of atherosclerosis. This suggests that crosstalk between lipid metabolism and innate immunity pathways plays an important role for the development and/or the prevention of atherosclerosis. However, it is not fully defined how innate immunity affects lipid metabolism. Macrophages play a central role in atherogenesis through the accumulation of cholesterol and the production of inflammatory mediators and cytokines. Liver X receptors (LXRs) exert an important atheroprotective effect in the macrophage. In addition to regulating cholesterol metabolism, LXRs are also negative regulators of macrophage inflammatory gene responses. In this review, we will discuss the roles of LXRs in the macrophage as key factors that link innate immunity and lipid metabolism.
Supplementary key words liver X receptors lipopolysaccharide low density lipoprotein Abbreviations: ABCA1, ATP binding cassette transporter A1; ABCG1, ATP binding cassette transporter G1; iNOS, inducible nitric oxide synthase; IRF3, interferon regulatory factor 3; LBP, LPS binding protein; LPS, lipopolysaccharide; LXR, liver X receptor; MyD88, myeloid differentiation factor 88; NF-
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