PortalPublikationenRole of Factor XII in hemostasis and thrombosis

Role of Factor XII in hemostasis and thrombosis

Standard

Role of Factor XII in hemostasis and thrombosis : clinical implications. / Renné, Thomas; Gailani, David.

in: EXPERT REV CARDIOVAS, Jahrgang 5, Nr. 4, 01.07.2007, S. 733-41.

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

Harvard

Renné, T & Gailani, D 2007, 'Role of Factor XII in hemostasis and thrombosis: clinical implications', EXPERT REV CARDIOVAS, Jg. 5, Nr. 4, S. 733-41. https://doi.org/10.1586/14779072.5.4.733

APA

Renné, T., & Gailani, D. (2007). Role of Factor XII in hemostasis and thrombosis: clinical implications. EXPERT REV CARDIOVAS, 5(4), 733-41. https://doi.org/10.1586/14779072.5.4.733

Vancouver

Renné T, Gailani D. Role of Factor XII in hemostasis and thrombosis: clinical implications. EXPERT REV CARDIOVAS. 2007 Jul 1;5(4):733-41. https://doi.org/10.1586/14779072.5.4.733

Bibtex

@article{ab31b5db41b1495d97dd2132468f643b,
title = "Role of Factor XII in hemostasis and thrombosis: clinical implications",
abstract = "The plasma coagulation system reacts quickly to limit blood loss from injury sites but also contributes to vascular thrombosis. In current models of hemostatic balance, normal coagulation and thrombosis represent two sides of the same coin, however, recent data from gene-deleted murine models have challenged this dogma. Deficiency of coagulation Factor XII (Hageman factor), a serine protease that initiates the intrinsic pathway of coagulation, severely impairs arterial thrombus formation but is not associated with excessive bleeding. These findings suggest that fibrin-generating mechanisms that operate during pathologic thrombus formation involve pathways distinct from those that are active during normal hemostasis. As Factor XII selectively contributes to thrombus formation in occlusive disease, but not to normal hemostasis, inhibition of this protease may offer a novel treatment strategy for prevention of arterial thrombosis with minimal or no risk of bleeding.",
keywords = "Angiotensin-Converting Enzyme Inhibitors, Animals, Blood Coagulation, Blood Coagulation Tests, Factor XII, Factor XII Deficiency, Fibrinolysis, Hemostasis, Humans, Kallikreins, Platelet Activation, Reperfusion Injury, Thrombin, Thrombosis",
author = "Thomas Renn{\'e} and David Gailani",
year = "2007",
month = jul,
day = "1",
doi = "10.1586/14779072.5.4.733",
language = "English",
volume = "5",
pages = "733--41",
journal = "EXPERT REV CARDIOVAS",
issn = "1477-9072",
publisher = "Taylor and Francis Ltd.",
number = "4",

}

RIS

TY - JOUR

T1 - Role of Factor XII in hemostasis and thrombosis

T2 - clinical implications

AU - Renné, Thomas

AU - Gailani, David

PY - 2007/7/1

Y1 - 2007/7/1

N2 - The plasma coagulation system reacts quickly to limit blood loss from injury sites but also contributes to vascular thrombosis. In current models of hemostatic balance, normal coagulation and thrombosis represent two sides of the same coin, however, recent data from gene-deleted murine models have challenged this dogma. Deficiency of coagulation Factor XII (Hageman factor), a serine protease that initiates the intrinsic pathway of coagulation, severely impairs arterial thrombus formation but is not associated with excessive bleeding. These findings suggest that fibrin-generating mechanisms that operate during pathologic thrombus formation involve pathways distinct from those that are active during normal hemostasis. As Factor XII selectively contributes to thrombus formation in occlusive disease, but not to normal hemostasis, inhibition of this protease may offer a novel treatment strategy for prevention of arterial thrombosis with minimal or no risk of bleeding.

AB - The plasma coagulation system reacts quickly to limit blood loss from injury sites but also contributes to vascular thrombosis. In current models of hemostatic balance, normal coagulation and thrombosis represent two sides of the same coin, however, recent data from gene-deleted murine models have challenged this dogma. Deficiency of coagulation Factor XII (Hageman factor), a serine protease that initiates the intrinsic pathway of coagulation, severely impairs arterial thrombus formation but is not associated with excessive bleeding. These findings suggest that fibrin-generating mechanisms that operate during pathologic thrombus formation involve pathways distinct from those that are active during normal hemostasis. As Factor XII selectively contributes to thrombus formation in occlusive disease, but not to normal hemostasis, inhibition of this protease may offer a novel treatment strategy for prevention of arterial thrombosis with minimal or no risk of bleeding.

KW - Angiotensin-Converting Enzyme Inhibitors

KW - Animals

KW - Blood Coagulation

KW - Blood Coagulation Tests

KW - Factor XII

KW - Factor XII Deficiency

KW - Fibrinolysis

KW - Hemostasis

KW - Humans

KW - Kallikreins

KW - Platelet Activation

KW - Reperfusion Injury

KW - Thrombin

KW - Thrombosis

U2 - 10.1586/14779072.5.4.733

DO - 10.1586/14779072.5.4.733

M3 - SCORING: Journal article

C2 - 17605651

VL - 5

SP - 733

EP - 741

JO - EXPERT REV CARDIOVAS

JF - EXPERT REV CARDIOVAS

SN - 1477-9072

IS - 4

ER -