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动脉粥样硬化中的巨噬细胞死亡和炎症消退缺陷。

Macrophage death and defective inflammation resolution in atherosclerosis.

机构信息

Department of Medicine, Physiology and Cellular Biophysics, Columbia University, New York, New York 10032, USA.

出版信息

Nat Rev Immunol. 2010 Jan;10(1):36-46. doi: 10.1038/nri2675. Epub 2009 Dec 4.

DOI:10.1038/nri2675
PMID:19960040
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2854623/
Abstract

A key event in atherosclerosis is a maladaptive inflammatory response to subendothelial lipoproteins. A crucial aspect of this response is a failure to resolve inflammation, which normally involves the suppression of inflammatory cell influx, effective clearance of apoptotic cells and promotion of inflammatory cell egress. Defects in these processes promote the progression of atherosclerotic lesions into dangerous plaques, which can trigger atherothrombotic vascular disease, the leading cause of death in industrialized societies. In this Review I provide an overview of these concepts, with a focus on macrophage death and defective apoptotic cell clearance, and discuss new therapeutic strategies designed to boost inflammation resolution in atherosclerosis.

摘要

动脉粥样硬化的一个关键事件是对血管内皮下脂蛋白的适应性炎症反应。这种反应的一个关键方面是炎症无法解决,这通常涉及抑制炎症细胞的流入、有效清除凋亡细胞和促进炎症细胞的流出。这些过程的缺陷会促进动脉粥样硬化病变向危险斑块的进展,从而引发动脉粥样硬化血栓形成性血管疾病,这是工业化社会中死亡的主要原因。在这篇综述中,我概述了这些概念,重点讨论了巨噬细胞死亡和凋亡细胞清除缺陷,并讨论了旨在增强动脉粥样硬化炎症解决的新治疗策略。

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本文引用的文献

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Role of ERO1-alpha-mediated stimulation of inositol 1,4,5-triphosphate receptor activity in endoplasmic reticulum stress-induced apoptosis.内质网应激诱导凋亡中ERO1-α介导的肌醇1,4,5-三磷酸受体活性刺激的作用
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Calcium/calmodulin-dependent protein kinase II links ER stress with Fas and mitochondrial apoptosis pathways.钙/钙调蛋白依赖性蛋白激酶 II 将内质网应激与 Fas 和线粒体凋亡途径联系起来。
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Macrophage diversity and polarization in atherosclerosis: a question of balance.动脉粥样硬化中的巨噬细胞多样性与极化:一个平衡问题。
Arterioscler Thromb Vasc Biol. 2009 Oct;29(10):1419-23. doi: 10.1161/ATVBAHA.108.180497. Epub 2009 Aug 20.
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Macrophage suppression following phagocytosis of apoptotic neutrophils is mediated by the S100A9 calcium-binding protein.吞噬凋亡中性粒细胞后巨噬细胞的抑制是由 S100A9 钙结合蛋白介导的。
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Apoptotic cells promote their own clearance and immune tolerance through activation of the nuclear receptor LXR.凋亡细胞通过激活核受体LXR促进自身清除和免疫耐受。
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Genetic deficiency and pharmacological stabilization of mast cells reduce diet-induced obesity and diabetes in mice.肥大细胞的基因缺陷和药物稳定作用可减轻小鼠饮食诱导的肥胖和糖尿病。
Nat Med. 2009 Aug;15(8):940-5. doi: 10.1038/nm.1994. Epub 2009 Jul 26.
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Circ Res. 2009 Aug 14;105(4):393-401. doi: 10.1161/CIRCRESAHA.109.201855. Epub 2009 Jul 23.
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