Neutrophil Extracellular Trap (NET) Impact on Deep Vein Thrombosis
Author(s) -
Tobias A. Fuchs,
Alexander Brill,
Denisa D. Wagner
Publication year - 2012
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.111.242859
Subject(s) - neutrophil extracellular traps , thrombosis , thrombus , medicine , von willebrand factor , coagulation , fibrin , platelet , deep vein , platelet activation , hemostasis , immunology , endothelium , inflammation , thrombolysis , myocardial infarction
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.
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