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Neutrophil extracellular trap (NET) impact on deep vein thrombosis

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Neutrophil extracellular trap (NET) impact on deep vein thrombosis. / Fuchs, Tobias A; Brill, Alexander; Wagner, Denisa D.

in: ARTERIOSCL THROM VAS, Jahrgang 32, Nr. 8, 01.08.2012, S. 1777-83.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Fuchs, TA, Brill, A & Wagner, DD 2012, 'Neutrophil extracellular trap (NET) impact on deep vein thrombosis', ARTERIOSCL THROM VAS, Jg. 32, Nr. 8, S. 1777-83. https://doi.org/10.1161/ATVBAHA.111.242859

APA

Fuchs, T. A., Brill, A., & Wagner, D. D. (2012). Neutrophil extracellular trap (NET) impact on deep vein thrombosis. ARTERIOSCL THROM VAS, 32(8), 1777-83. https://doi.org/10.1161/ATVBAHA.111.242859

Vancouver

Fuchs TA, Brill A, Wagner DD. Neutrophil extracellular trap (NET) impact on deep vein thrombosis. ARTERIOSCL THROM VAS. 2012 Aug 1;32(8):1777-83. https://doi.org/10.1161/ATVBAHA.111.242859

Bibtex

@article{ae43c8c076a44af7b5e19df8fad48b30,
title = "Neutrophil extracellular trap (NET) impact on deep vein thrombosis",
abstract = "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.",
keywords = "Animals, Blood Coagulation, Blood Platelets, Disease Models, Animal, Endothelium, Vascular, Erythrocytes, Humans, Immunity, Innate, Mechanical Thrombolysis, Neutrophils, Thromboplastin, Venous Thrombosis",
author = "Fuchs, {Tobias A} and Alexander Brill and Wagner, {Denisa D}",
year = "2012",
month = aug,
day = "1",
doi = "10.1161/ATVBAHA.111.242859",
language = "English",
volume = "32",
pages = "1777--83",
journal = "ARTERIOSCL THROM VAS",
issn = "1079-5642",
publisher = "Lippincott Williams and Wilkins",
number = "8",

}

RIS

TY - JOUR

T1 - Neutrophil extracellular trap (NET) impact on deep vein thrombosis

AU - Fuchs, Tobias A

AU - Brill, Alexander

AU - Wagner, Denisa D

PY - 2012/8/1

Y1 - 2012/8/1

N2 - 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.

AB - 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.

KW - Animals

KW - Blood Coagulation

KW - Blood Platelets

KW - Disease Models, Animal

KW - Endothelium, Vascular

KW - Erythrocytes

KW - Humans

KW - Immunity, Innate

KW - Mechanical Thrombolysis

KW - Neutrophils

KW - Thromboplastin

KW - Venous Thrombosis

U2 - 10.1161/ATVBAHA.111.242859

DO - 10.1161/ATVBAHA.111.242859

M3 - SCORING: Journal article

C2 - 22652600

VL - 32

SP - 1777

EP - 1783

JO - ARTERIOSCL THROM VAS

JF - ARTERIOSCL THROM VAS

SN - 1079-5642

IS - 8

ER -