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Circulating Extracellular DNA

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Circulating Extracellular DNA : Cause or Consequence of Thrombosis? / Jiménez-Alcázar, Miguel; Kim, Natalie; Fuchs, Tobias A.

in: SEMIN THROMB HEMOST, Jahrgang 43, Nr. 6, 09.2017, S. 553-561.

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

Harvard

Jiménez-Alcázar, M, Kim, N & Fuchs, TA 2017, 'Circulating Extracellular DNA: Cause or Consequence of Thrombosis?', SEMIN THROMB HEMOST, Jg. 43, Nr. 6, S. 553-561. https://doi.org/10.1055/s-0036-1597284

APA

Jiménez-Alcázar, M., Kim, N., & Fuchs, T. A. (2017). Circulating Extracellular DNA: Cause or Consequence of Thrombosis? SEMIN THROMB HEMOST, 43(6), 553-561. https://doi.org/10.1055/s-0036-1597284

Vancouver

Jiménez-Alcázar M, Kim N, Fuchs TA. Circulating Extracellular DNA: Cause or Consequence of Thrombosis? SEMIN THROMB HEMOST. 2017 Sep;43(6):553-561. https://doi.org/10.1055/s-0036-1597284

Bibtex

@article{f27d11e1c11e4b859b867aa42ea82f16,
title = "Circulating Extracellular DNA: Cause or Consequence of Thrombosis?",
abstract = "Thrombosis leads to ischemic organ damage in cardiovascular and thromboembolic diseases. Neutrophils promote thrombosis in vitro and in vivo by releasing neutrophil extracellular traps (NETs). NETs are composed of DNA filaments coated with histones and neutrophil enzymes such as myeloperoxidase (MPO). Circulating extracellular DNA (ceDNA) is widely used as a surrogate marker to monitor NET formation in thrombosis. This narrative review summarizes the association of ceDNA with human thrombosis. Levels of ceDNA indicate the extent and outcome of several cardiovascular and thromboembolic diseases, including myocardial infarction, stroke, and venous thromboembolism. ceDNA correlates with markers of coagulation and platelet consumption, thus supporting the hypothesis that ceDNA may be a surrogate marker of thrombus formation. In addition, ceDNA levels correlate with markers of cell injury and size of ischemic lesions, suggesting that ceDNA does not derive from NETs but is probably released from damaged organs. Few studies identified NET-specific biomarkers such as DNA-MPO complexes in the blood of patients with thrombosis. In conclusion, it remains to be established whether ceDNA in patients derives from NETs and is a cause or consequence of thrombosis.",
keywords = "Journal Article",
author = "Miguel Jim{\'e}nez-Alc{\'a}zar and Natalie Kim and Fuchs, {Tobias A}",
note = "Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.",
year = "2017",
month = sep,
doi = "10.1055/s-0036-1597284",
language = "English",
volume = "43",
pages = "553--561",
journal = "SEMIN THROMB HEMOST",
issn = "0094-6176",
publisher = "Thieme Medical Publishers",
number = "6",

}

RIS

TY - JOUR

T1 - Circulating Extracellular DNA

T2 - Cause or Consequence of Thrombosis?

AU - Jiménez-Alcázar, Miguel

AU - Kim, Natalie

AU - Fuchs, Tobias A

N1 - Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

PY - 2017/9

Y1 - 2017/9

N2 - Thrombosis leads to ischemic organ damage in cardiovascular and thromboembolic diseases. Neutrophils promote thrombosis in vitro and in vivo by releasing neutrophil extracellular traps (NETs). NETs are composed of DNA filaments coated with histones and neutrophil enzymes such as myeloperoxidase (MPO). Circulating extracellular DNA (ceDNA) is widely used as a surrogate marker to monitor NET formation in thrombosis. This narrative review summarizes the association of ceDNA with human thrombosis. Levels of ceDNA indicate the extent and outcome of several cardiovascular and thromboembolic diseases, including myocardial infarction, stroke, and venous thromboembolism. ceDNA correlates with markers of coagulation and platelet consumption, thus supporting the hypothesis that ceDNA may be a surrogate marker of thrombus formation. In addition, ceDNA levels correlate with markers of cell injury and size of ischemic lesions, suggesting that ceDNA does not derive from NETs but is probably released from damaged organs. Few studies identified NET-specific biomarkers such as DNA-MPO complexes in the blood of patients with thrombosis. In conclusion, it remains to be established whether ceDNA in patients derives from NETs and is a cause or consequence of thrombosis.

AB - Thrombosis leads to ischemic organ damage in cardiovascular and thromboembolic diseases. Neutrophils promote thrombosis in vitro and in vivo by releasing neutrophil extracellular traps (NETs). NETs are composed of DNA filaments coated with histones and neutrophil enzymes such as myeloperoxidase (MPO). Circulating extracellular DNA (ceDNA) is widely used as a surrogate marker to monitor NET formation in thrombosis. This narrative review summarizes the association of ceDNA with human thrombosis. Levels of ceDNA indicate the extent and outcome of several cardiovascular and thromboembolic diseases, including myocardial infarction, stroke, and venous thromboembolism. ceDNA correlates with markers of coagulation and platelet consumption, thus supporting the hypothesis that ceDNA may be a surrogate marker of thrombus formation. In addition, ceDNA levels correlate with markers of cell injury and size of ischemic lesions, suggesting that ceDNA does not derive from NETs but is probably released from damaged organs. Few studies identified NET-specific biomarkers such as DNA-MPO complexes in the blood of patients with thrombosis. In conclusion, it remains to be established whether ceDNA in patients derives from NETs and is a cause or consequence of thrombosis.

KW - Journal Article

U2 - 10.1055/s-0036-1597284

DO - 10.1055/s-0036-1597284

M3 - SCORING: Journal article

C2 - 28359134

VL - 43

SP - 553

EP - 561

JO - SEMIN THROMB HEMOST

JF - SEMIN THROMB HEMOST

SN - 0094-6176

IS - 6

ER -