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Intrinsic pathway of coagulation and arterial thrombosis

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Intrinsic pathway of coagulation and arterial thrombosis. / Gailani, David; Renné, Thomas.

in: ARTERIOSCL THROM VAS, Jahrgang 27, Nr. 12, 01.12.2007, S. 2507-13.

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

Harvard

Gailani, D & Renné, T 2007, 'Intrinsic pathway of coagulation and arterial thrombosis', ARTERIOSCL THROM VAS, Jg. 27, Nr. 12, S. 2507-13. https://doi.org/10.1161/ATVBAHA.107.155952

APA

Gailani, D., & Renné, T. (2007). Intrinsic pathway of coagulation and arterial thrombosis. ARTERIOSCL THROM VAS, 27(12), 2507-13. https://doi.org/10.1161/ATVBAHA.107.155952

Vancouver

Gailani D, Renné T. Intrinsic pathway of coagulation and arterial thrombosis. ARTERIOSCL THROM VAS. 2007 Dez 1;27(12):2507-13. https://doi.org/10.1161/ATVBAHA.107.155952

Bibtex

@article{b975c32b3cc74dbba2efc89ccf9e98e2,
title = "Intrinsic pathway of coagulation and arterial thrombosis",
abstract = "Formation of a fibrin clot is mediated by a group of tightly regulated plasma proteases and cofactors. While this system is essential for minimizing blood loss from an injured blood vessel (hemostasis), it also contributes to pathologic fibrin formation and platelet activation that may occlude vessels (thrombosis). Many antithrombotic drugs target key elements of the plasma coagulation mechanism such as thrombin and factor Xa, based on the premise that plasma elements contributing to thrombosis are primarily those involved in hemostasis. Recent studies with genetically altered mice raise questions about this paradigm. Deficiencies of the intrinsic pathway proteases factor XII and factor XI are not associated with abnormal hemostasis in mice, but impair formation of occlusive thrombi in arterial injury models, indicating that pathways not essential for hemostasis participate in arterial thrombosis. If factor XII or factor XI make similar contributions to thrombosis in humans, these proteases could be ideal targets for drugs to treat or prevent thromboembolic disease with minimal risk of therapy-associated bleeding.",
keywords = "Animals, Anticoagulants, Blood Coagulation, Disease Models, Animal, Factor XI, Factor XI Deficiency, Factor XII, Factor XII Deficiency, Fibrin, Hemostasis, Humans, Infarction, Middle Cerebral Artery, Mice, Mice, Knockout, Protease Inhibitors, Reperfusion Injury, Thromboembolism, Thrombosis",
author = "David Gailani and Thomas Renn{\'e}",
year = "2007",
month = dec,
day = "1",
doi = "10.1161/ATVBAHA.107.155952",
language = "English",
volume = "27",
pages = "2507--13",
journal = "ARTERIOSCL THROM VAS",
issn = "1079-5642",
publisher = "Lippincott Williams and Wilkins",
number = "12",

}

RIS

TY - JOUR

T1 - Intrinsic pathway of coagulation and arterial thrombosis

AU - Gailani, David

AU - Renné, Thomas

PY - 2007/12/1

Y1 - 2007/12/1

N2 - Formation of a fibrin clot is mediated by a group of tightly regulated plasma proteases and cofactors. While this system is essential for minimizing blood loss from an injured blood vessel (hemostasis), it also contributes to pathologic fibrin formation and platelet activation that may occlude vessels (thrombosis). Many antithrombotic drugs target key elements of the plasma coagulation mechanism such as thrombin and factor Xa, based on the premise that plasma elements contributing to thrombosis are primarily those involved in hemostasis. Recent studies with genetically altered mice raise questions about this paradigm. Deficiencies of the intrinsic pathway proteases factor XII and factor XI are not associated with abnormal hemostasis in mice, but impair formation of occlusive thrombi in arterial injury models, indicating that pathways not essential for hemostasis participate in arterial thrombosis. If factor XII or factor XI make similar contributions to thrombosis in humans, these proteases could be ideal targets for drugs to treat or prevent thromboembolic disease with minimal risk of therapy-associated bleeding.

AB - Formation of a fibrin clot is mediated by a group of tightly regulated plasma proteases and cofactors. While this system is essential for minimizing blood loss from an injured blood vessel (hemostasis), it also contributes to pathologic fibrin formation and platelet activation that may occlude vessels (thrombosis). Many antithrombotic drugs target key elements of the plasma coagulation mechanism such as thrombin and factor Xa, based on the premise that plasma elements contributing to thrombosis are primarily those involved in hemostasis. Recent studies with genetically altered mice raise questions about this paradigm. Deficiencies of the intrinsic pathway proteases factor XII and factor XI are not associated with abnormal hemostasis in mice, but impair formation of occlusive thrombi in arterial injury models, indicating that pathways not essential for hemostasis participate in arterial thrombosis. If factor XII or factor XI make similar contributions to thrombosis in humans, these proteases could be ideal targets for drugs to treat or prevent thromboembolic disease with minimal risk of therapy-associated bleeding.

KW - Animals

KW - Anticoagulants

KW - Blood Coagulation

KW - Disease Models, Animal

KW - Factor XI

KW - Factor XI Deficiency

KW - Factor XII

KW - Factor XII Deficiency

KW - Fibrin

KW - Hemostasis

KW - Humans

KW - Infarction, Middle Cerebral Artery

KW - Mice

KW - Mice, Knockout

KW - Protease Inhibitors

KW - Reperfusion Injury

KW - Thromboembolism

KW - Thrombosis

U2 - 10.1161/ATVBAHA.107.155952

DO - 10.1161/ATVBAHA.107.155952

M3 - SCORING: Journal article

C2 - 17916770

VL - 27

SP - 2507

EP - 2513

JO - ARTERIOSCL THROM VAS

JF - ARTERIOSCL THROM VAS

SN - 1079-5642

IS - 12

ER -