Neutrophil Extracellular Traps Participate in Cardiovascular Diseases Recent Experimental and Clinical Insights
Neutrophil Extracellular Traps Participate in Cardiovascular Diseases Recent Experimental and Clinical Insights
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DOI：
10.1161/circresaha.120.315931
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发表时间：
2020-04-24
影响因子：
20.1
通讯作者：
Soehnlein, Oliver
中科院分区：
文献类型：
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作者：
Doering, Yvonne;Libby, Peter;Soehnlein, Oliver
神经细胞外陷阱（NET）最近已成为一个新认识的贡献者静脉和动脉血栓形成。这些DNA链被激活或垂死的中性粒细胞挤出，用各种蛋白质介质装饰，成为固态反应器，可以定位在血液与患病动脉内膜表面的关键界面处，并传播和放大区域损伤。因此，NET提供了炎症，先天免疫，血栓形成，氧化应激和心血管疾病之间的联系。在对疾病相关刺激的反应中，中性粒细胞经历一系列特定的反应，最终形成NET。来自细胞核或线粒体的DNA可以促进NET的形成。从嗜中性粒细胞释放的DNA形成网状网，在形态上类似于网，使得首字母缩略词NETs特别合适。NET的DNA骨架不仅呈递固有的中性粒细胞蛋白（例如，MPO [髓过氧化物酶]和各种蛋白酶），而且可以聚集血液中发现的其他蛋白（例如，组织因子促凝剂）。本文综述了目前中性粒细胞生物学的概念，NET形成的触发因素和机制，以及NET对动脉粥样硬化和血栓形成的贡献。我们考虑在临床研究中使用NET的标记物。我们的目标是批判性地整合实验文献与越来越多的临床信息有关NET。
Neutrophil extracellular traps (NETs) have recently emerged as a newly recognized contributor to venous and arterial thrombosis. These strands of DNA extruded by activated or dying neutrophils, decorated with various protein mediators, become solid-state reactors that can localize at the critical interface of blood with the intimal surface of diseased arteries and propagate and amplify the regional injury. NETs thus furnish a previously unsuspected link between inflammation, innate immunity, thrombosis, oxidative stress, and cardiovascular diseases. In response to disease-relevant stimuli, neutrophils undergo a specialized series of reactions that culminate in NET formation. DNA derived from either nuclei or mitochondria can contribute to NET formation. The DNA liberated from neutrophils forms a reticular mesh that resembles morphologically a net, rendering the acronym NETs particularly appropriate. The DNA backbone of NETs not only presents intrinsic neutrophil proteins (eg, MPO [myeloperoxidase] and various proteinases) but can gather other proteins found in blood (eg, tissue factor procoagulant). This review presents current concepts of neutrophil biology, the triggers to and mechanisms of NET formation, and the contribution of NETs to atherosclerosis and to thrombosis. We consider the use of markers of NETs in clinical studies. We aim here to integrate critically the experimental literature with the growing body of clinical information regarding NETs.