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本文引用的文献

1
Nascent HDL formation by hepatocytes is reduced by the concerted action of serum amyloid A and endothelial lipase.肝细胞新生高密度脂蛋白的形成会被血清淀粉样蛋白 A 和内皮脂肪酶的协同作用所减少。
J Lipid Res. 2011 Dec;52(12):2255-2261. doi: 10.1194/jlr.M017681. Epub 2011 Sep 27.
2
Anti-atherogenic mechanisms of high density lipoprotein: effects on myeloid cells.高密度脂蛋白的抗动脉粥样硬化机制:对髓细胞的影响。
Biochim Biophys Acta. 2012 Mar;1821(3):513-21. doi: 10.1016/j.bbalip.2011.08.003. Epub 2011 Aug 16.
3
Plasma PLTP (phospholipid-transfer protein): an emerging role in 'reverse lipopolysaccharide transport' and innate immunity.血浆 PLTP(磷脂转运蛋白):在“反向脂多糖转运”和先天免疫中的新作用。
Biochem Soc Trans. 2011 Aug;39(4):984-8. doi: 10.1042/BST0390984.
4
Interleukin-6 protects human macrophages from cellular cholesterol accumulation and attenuates the proinflammatory response.白细胞介素-6 可保护人巨噬细胞免受细胞胆固醇蓄积,并减弱促炎反应。
J Biol Chem. 2011 Sep 2;286(35):30926-30936. doi: 10.1074/jbc.M111.264325. Epub 2011 Jul 8.
5
Autophagy regulates cholesterol efflux from macrophage foam cells via lysosomal acid lipase.自噬通过溶酶体酸性脂肪酶调节巨噬细胞泡沫细胞中的胆固醇外流。
Cell Metab. 2011 Jun 8;13(6):655-67. doi: 10.1016/j.cmet.2011.03.023.
6
The role of microRNAs in cholesterol efflux and hepatic lipid metabolism.microRNAs 在胆固醇外排和肝脏脂质代谢中的作用。
Annu Rev Nutr. 2011 Aug 21;31:49-63. doi: 10.1146/annurev-nutr-081810-160756.
7
Impact of HDL oxidation by the myeloperoxidase system on sterol efflux by the ABCA1 pathway.髓过氧化物酶系统对高密度脂蛋白的氧化作用对 ABCA1 途径的固醇外流的影响。
J Proteomics. 2011 Oct 19;74(11):2289-99. doi: 10.1016/j.jprot.2011.04.001. Epub 2011 Apr 9.
8
Friend Turns Foe: Transformation of Anti-Inflammatory HDL to Proinflammatory HDL during Acute-Phase Response.朋友变敌人:急性期反应期间抗炎性高密度脂蛋白向促炎性高密度脂蛋白的转变
Cholesterol. 2011;2011:274629. doi: 10.1155/2011/274629. Epub 2010 Nov 25.
9
Role of hepatic lipase and endothelial lipase in high-density lipoprotein-mediated reverse cholesterol transport.肝脂肪酶和内皮脂肪酶在高密度脂蛋白介导的胆固醇逆转运中的作用。
Curr Atheroscler Rep. 2011 Jun;13(3):257-65. doi: 10.1007/s11883-011-0175-2.
10
Host defense against viral infection involves interferon mediated down-regulation of sterol biosynthesis.宿主防御病毒感染涉及干扰素介导的固醇生物合成下调。
PLoS Biol. 2011 Mar;9(3):e1000598. doi: 10.1371/journal.pbio.1000598. Epub 2011 Mar 8.

胆固醇逆转运与固有免疫的相互作用。

Crosstalk between reverse cholesterol transport and innate immunity.

机构信息

Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.

出版信息

Trends Endocrinol Metab. 2012 Apr;23(4):169-78. doi: 10.1016/j.tem.2012.02.001. Epub 2012 Mar 10.

DOI:10.1016/j.tem.2012.02.001
PMID:22406271
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3338129/
Abstract

Although lipid metabolism and host defense are widely considered to be very divergent disciplines, compelling evidence suggests that host cell handling of self- and microbe-derived (e.g. lipopolysaccharide, LPS) lipids may have common evolutionary roots, and that they indeed may be inseparable processes. The innate immune response and the homeostatic network controlling cellular sterol levels are now known to regulate each other reciprocally, with important implications for several common diseases, including atherosclerosis. In the present review we discuss recent discoveries that provide new insight into the bidirectional crosstalk between reverse cholesterol transport and innate immunity, and highlight the broader implications of these findings for the development of therapeutics.

摘要

尽管脂质代谢和宿主防御被广泛认为是非常不同的学科,但有确凿的证据表明,宿主细胞处理自身和微生物来源的(例如脂多糖,LPS)脂质可能具有共同的进化根源,实际上它们可能是不可分割的过程。先天免疫反应和控制细胞固醇水平的动态平衡网络现在被认为是相互调节的,这对几种常见疾病(包括动脉粥样硬化)有重要影响。在本综述中,我们讨论了最近的发现,这些发现为胆固醇逆向转运和先天免疫之间的双向相互作用提供了新的见解,并强调了这些发现对治疗药物开发的更广泛意义。