Neutrophil Extracellular Trap (NET) Impact on Deep Vein ThrombosisTobias

被引：428
作者：
Fuchs, Tobias A.
Brill, Alexander
Wagner, Denisa D. [1 ]
机构：
[1] Immune Dis Inst, Boston, MA 02115 USA
来源：
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY | 2012年 / 32卷 / 08期
基金：
美国国家卫生研究院;
关键词：
deep vein thrombosis; deoxyribonuclease; inflammation; mouse model; neutrophil extracellular traps; thrombolytic therapy; VON-WILLEBRAND-FACTOR; PULMONARY-EMBOLISM; VENOUS THROMBOSIS; LEUKOCYTE ELASTASE; MITOCHONDRIAL-DNA; ENDOTHELIAL-CELLS; INNATE IMMUNITY; HUMAN-PLATELETS; CANCER-PATIENTS; RISK-FACTORS;
D O I：
10.1161/ATVBAHA.111.242859
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Deep vein thrombosis (DVT) is a major health problem that requires improved prophylaxis and treatment. Inflammatory conditions such as infection, cancer, and autoimmune diseases are risk factors for DVT. We and others have recently shown that extracellular DNA fibers produced in inflammation and known as neutrophil extracellular traps (NETs) contribute to experimental DVT. NETs stimulate thrombus formation and coagulation and are abundant in thrombi in animal models of DVT. It appears that, in addition to fibrin and von Willebrand factor, NETs represent a third thrombus scaffold. Here, we review how NETs stimulate thrombosis and discuss known and potential interactions of NETs with endothelium, platelets, red blood cells, and coagulation factors and how NETs could influence thrombolysis. We propose that drugs that inhibit NET formation or facilitate NET degradation may prevent or treat DVT. (Arterioscler Thromb Vasc Biol. 2012;32:1777-1783.)
引用
收藏
页码：1777 / 1783
页数：7
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