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The Ins and Outs of Myeloid Cells in Atherosclerosis.动脉粥样硬化中骨髓细胞的来龙去脉。
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Atherosclerosis - A matter of unresolved inflammation.动脉粥样硬化——一个炎症未得到解决的问题。
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本文引用的文献

1
Visualizing the function and fate of neutrophils in sterile injury and repair.可视化中性粒细胞在非感染性损伤和修复中的功能和命运。
Science. 2017 Oct 6;358(6359):111-116. doi: 10.1126/science.aam9690.
2
Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease.卡那奴单抗治疗动脉粥样硬化疾病的抗炎疗法。
N Engl J Med. 2017 Sep 21;377(12):1119-1131. doi: 10.1056/NEJMoa1707914. Epub 2017 Aug 27.
3
Inflammatory Ly6Chi monocytes and their conversion to M2 macrophages drive atherosclerosis regression.炎症性Ly6Chi单核细胞及其向M2巨噬细胞的转化驱动动脉粥样硬化消退。
J Clin Invest. 2017 Aug 1;127(8):2904-2915. doi: 10.1172/JCI75005. Epub 2017 Jun 26.
4
Endothelial Protective Monocyte Patrolling in Large Arteries Intensified by Western Diet and Atherosclerosis.西方饮食和动脉粥样硬化加剧大动脉中内皮保护性单核细胞的巡逻
Circ Res. 2017 May 26;120(11):1789-1799. doi: 10.1161/CIRCRESAHA.117.310739. Epub 2017 Mar 16.
5
Chemokine binding protein 'M3' limits atherosclerosis in apolipoprotein E-/- mice.趋化因子结合蛋白“M3”可限制载脂蛋白E基因敲除小鼠的动脉粥样硬化。
PLoS One. 2017 Mar 10;12(3):e0173224. doi: 10.1371/journal.pone.0173224. eCollection 2017.
6
The phenomenon of atherosclerosis reversal and regression: Lessons from animal models.动脉粥样硬化逆转与消退现象:来自动物模型的经验教训。
Exp Mol Pathol. 2017 Feb;102(1):138-145. doi: 10.1016/j.yexmp.2017.01.013. Epub 2017 Jan 17.
7
Cathepsin G Controls Arterial But Not Venular Myeloid Cell Recruitment.组织蛋白酶G控制动脉而非静脉的髓样细胞募集。
Circulation. 2016 Oct 18;134(16):1176-1188. doi: 10.1161/CIRCULATIONAHA.116.024790. Epub 2016 Sep 22.
8
An imbalance between specialized pro-resolving lipid mediators and pro-inflammatory leukotrienes promotes instability of atherosclerotic plaques.促分解脂质介质与促炎白三烯之间的失衡会促进动脉粥样硬化斑块的不稳定。
Nat Commun. 2016 Sep 23;7:12859. doi: 10.1038/ncomms12859.
9
Resolving Lipid Mediators Maresin 1 and Resolvin D2 Prevent Atheroprogression in Mice.解决脂质介质maresin 1 和 resolvin D2 可预防小鼠动脉粥样硬化进展。
Circ Res. 2016 Oct 14;119(9):1030-1038. doi: 10.1161/CIRCRESAHA.116.309492. Epub 2016 Aug 16.
10
RNAi targeting multiple cell adhesion molecules reduces immune cell recruitment and vascular inflammation after myocardial infarction.靶向多种细胞黏附分子的RNA干扰可减少心肌梗死后免疫细胞募集和血管炎症。
Sci Transl Med. 2016 Jun 8;8(342):342ra80. doi: 10.1126/scitranslmed.aaf1435.

动脉粥样硬化中骨髓细胞的来龙去脉。

The Ins and Outs of Myeloid Cells in Atherosclerosis.

机构信息

Institute for Cardiovascular Prevention (IPEK), Ludwig Maximilian University, Munich, Germany.

Institute for Cardiovascular Prevention (IPEK), Ludwig Maximilian University, Munich,

出版信息

J Innate Immun. 2018;10(5-6):479-486. doi: 10.1159/000488091. Epub 2018 Apr 18.

DOI:10.1159/000488091
PMID:29669334
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6784034/
Abstract

Atherosclerosis is a chronic inflammation of the arterial vessel wall that arises from an imbalanced lipid metabolism. A growing body of literature describes leukocyte recruitment as a critical step in the initiation and progression of lesion development. By contrast, the role of leukocytes during plaque regression has been described in less detail. Leukocyte egress might be an important step to resolving chronic inflammation and therefore it may be a promising target for limiting advanced lesion development. This review aims to summarize our current knowledge of leukocyte recruitment to the arterial vessel wall. We will discuss mechanisms of leukocyte egress from the lesion site, as well as potential therapeutic strategies to promote atherosclerotic regression.

摘要

动脉粥样硬化是一种动脉血管壁的慢性炎症,源于脂质代谢失衡。越来越多的文献描述了白细胞募集是病变发展起始和进展的关键步骤。相比之下,白细胞在斑块消退过程中的作用描述得较少。白细胞迁出可能是解决慢性炎症的重要步骤,因此它可能是限制晚期病变发展的一个有前途的靶点。这篇综述旨在总结我们目前对白细胞向动脉血管壁募集的认识。我们将讨论白细胞从病变部位迁出的机制,以及促进动脉粥样硬化消退的潜在治疗策略。