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本文引用的文献

1
Hypoxia-inducible factor 1 controls the expression of the uncoordinated-5-B receptor, but not of netrin-1, in first trimester human placenta.缺氧诱导因子1调控孕早期人胎盘中不协调蛋白5-B受体的表达,但不调控网蛋白1的表达。
Int J Dev Biol. 2011;55(10-12):981-7. doi: 10.1387/ijdb.103276md.
2
The neuroimmune guidance cue netrin-1 promotes atherosclerosis by inhibiting the emigration of macrophages from plaques.神经免疫导向分子 netrin-1 通过抑制斑块内巨噬细胞的迁移来促进动脉粥样硬化的形成。
Nat Immunol. 2012 Jan 8;13(2):136-43. doi: 10.1038/ni.2205.
3
Acidity and lipolysis by group V secreted phospholipase A(2) strongly increase the binding of apoB-100-containing lipoproteins to human aortic proteoglycans.V 组分泌型磷脂酶 A(2) 引起的酸度和脂解作用会显著增强含载脂蛋白 B-100 的脂蛋白与人类主动脉蛋白聚糖的结合。
Biochim Biophys Acta. 2012 Feb;1821(2):257-67. doi: 10.1016/j.bbalip.2011.10.014. Epub 2011 Oct 25.
4
Positive cross-talk between hypoxia inducible factor-1α and liver X receptor α induces formation of triglyceride-loaded foam cells.缺氧诱导因子-1α与肝 X 受体α之间的正对话诱导甘油三酯负荷泡沫细胞的形成。
Arterioscler Thromb Vasc Biol. 2011 Dec;31(12):2949-56. doi: 10.1161/ATVBAHA.111.235788. Epub 2011 Sep 22.
5
Hypoxia is present in murine atherosclerotic plaques and has multiple adverse effects on macrophage lipid metabolism.缺氧存在于鼠动脉粥样硬化斑块中,并对巨噬细胞脂质代谢产生多种不良影响。
Circ Res. 2011 Oct 28;109(10):1141-52. doi: 10.1161/CIRCRESAHA.111.246363. Epub 2011 Sep 15.
6
Detection of hypoxia by [18F]EF5 in atherosclerotic plaques in mice.通过 [18F]EF5 在小鼠动脉粥样硬化斑块中检测缺氧。
Arterioscler Thromb Vasc Biol. 2011 May;31(5):1011-5. doi: 10.1161/ATVBAHA.110.221440. Epub 2011 Mar 3.
7
Macrophages exposed to hypoxia secrete proteoglycans for which LDL has higher affinity.缺氧环境下的巨噬细胞会分泌蛋白聚糖,而 LDL 对其具有更高的亲和力。
Atherosclerosis. 2011 Mar;215(1):77-81. doi: 10.1016/j.atherosclerosis.2010.12.017. Epub 2010 Dec 23.
8
Free cholesterol-induced cytotoxicity a possible contributing factor to macrophage foam cell necrosis in advanced atherosclerotic lesions.游离胆固醇诱导的细胞毒性可能是晚期动脉粥样硬化病变中巨噬细胞泡沫细胞坏死的一个促成因素。
Trends Cardiovasc Med. 1997 Oct;7(7):256-63. doi: 10.1016/S1050-1738(97)00086-8.
9
The liver X receptor (LXR) and its target gene ABCA1 are regulated upon low oxygen in human trophoblast cells: a reason for alterations in preeclampsia?肝 X 受体 (LXR) 及其靶基因 ABCA1 在人滋养层细胞低氧时受到调节:子痫前期改变的原因?
Placenta. 2010 Oct;31(10):910-8. doi: 10.1016/j.placenta.2010.07.009. Epub 2010 Aug 14.
10
HIF-1beta determines ABCA1 expression under hypoxia in human macrophages.低氧环境下 HIF-1β调控人巨噬细胞 ABCA1 的表达。
Int J Biochem Cell Biol. 2010 Feb;42(2):241-52. doi: 10.1016/j.biocel.2009.10.002. Epub 2009 Oct 12.

小鼠动脉粥样硬化斑块中的缺氧及其对巨噬细胞的不良影响。

Hypoxia in murine atherosclerotic plaques and its adverse effects on macrophages.

机构信息

Department of Medicine (Cardiology), Marc and Ruti Bell Program in Vascular Biology, NYU School of Medicine, Smilow 7, 522 First Ave., New York, NY 10016, USA.

出版信息

Trends Cardiovasc Med. 2013 Apr;23(3):80-4. doi: 10.1016/j.tcm.2012.09.004. Epub 2013 Feb 1.

DOI:10.1016/j.tcm.2012.09.004
PMID:23375596
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3757341/
Abstract

Hypoxia has been found in the atherosclerotic plaques of larger mammals, including humans. Whether hypoxia occurs in the plaques of standard mouse models with atherosclerosis has been controversial, given their small size. In this review, we summarize the findings of a recent report demonstrating that direct evidence of hypoxia can indeed be found in the plaques of mice deficient in apolipoprotein E (apoE-/-mice). Furthermore, studies in vitro showed that hypoxia promoted lipid synthesis and reduced cholesterol efflux through the ABCA1 pathway, and that the transcription factor HIF-1α mediated many, but not all, of the effects. These results are discussed in the context of the literature and clinical practice.

摘要

缺氧已在大型哺乳动物的动脉粥样硬化斑块中被发现,包括人类。由于标准动脉粥样硬化小鼠模型体积较小,因此关于缺氧是否发生在这些斑块中一直存在争议。在这篇综述中,我们总结了最近一份报告的发现,该报告表明,载脂蛋白 E 缺陷(apoE-/-)小鼠的斑块中确实存在缺氧的直接证据。此外,体外研究表明,缺氧通过 ABCA1 途径促进脂质合成和减少胆固醇外排,转录因子 HIF-1α 介导了许多但不是所有的作用。这些结果在文献和临床实践的背景下进行了讨论。