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Factor XI and XII as antithrombotic targets.

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Factor XI and XII as antithrombotic targets. / Müller, Felicitas; Gailani, David; Renné, Thomas.

In: CURR OPIN HEMATOL, Vol. 18, No. 5, 5, 2011, p. 349-355.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Müller, F, Gailani, D & Renné, T 2011, 'Factor XI and XII as antithrombotic targets.', CURR OPIN HEMATOL, vol. 18, no. 5, 5, pp. 349-355. <http://www.ncbi.nlm.nih.gov/pubmed/21730835?dopt=Citation>

APA

Müller, F., Gailani, D., & Renné, T. (2011). Factor XI and XII as antithrombotic targets. CURR OPIN HEMATOL, 18(5), 349-355. [5]. http://www.ncbi.nlm.nih.gov/pubmed/21730835?dopt=Citation

Vancouver

Müller F, Gailani D, Renné T. Factor XI and XII as antithrombotic targets. CURR OPIN HEMATOL. 2011;18(5):349-355. 5.

Bibtex

@article{922bdfe551bc4126a20705afe22a2608,
title = "Factor XI and XII as antithrombotic targets.",
abstract = "Arterial and venous thrombosis are major causes of morbidity and mortality, and the incidence of thromboembolic diseases increases as a population ages. Thrombi are formed by activated platelets and fibrin. The latter is a product of the plasma coagulation system. Currently available anticoagulants such as heparins, vitamin K antagonists and inhibitors of thrombin or factor Xa target enzymes of the coagulation cascade that are critical for fibrin formation. However, fibrin is also necessary for terminating blood loss at sites of vascular injury. As a result, anticoagulants currently in clinical use increase the risk of bleeding, partially offsetting the benefits of reduced thrombosis. This review focuses on new targets for anticoagulation that are associated with minimal or no therapy-associated increased bleeding.",
keywords = "Animals, Humans, Anticoagulants/*pharmacology/therapeutic use, Blood Coagulation/drug effects/physiology, Factor XI/*antagonists & inhibitors/metabolism, Factor XI Deficiency/blood/drug therapy/metabolism, Factor XII/*antagonists & inhibitors/metabolism, Factor XII Deficiency/blood/drug therapy/metabolism, Hemostasis/drug effects/physiology, Thrombosis/*drug therapy/*metabolism, Animals, Humans, Anticoagulants/*pharmacology/therapeutic use, Blood Coagulation/drug effects/physiology, Factor XI/*antagonists & inhibitors/metabolism, Factor XI Deficiency/blood/drug therapy/metabolism, Factor XII/*antagonists & inhibitors/metabolism, Factor XII Deficiency/blood/drug therapy/metabolism, Hemostasis/drug effects/physiology, Thrombosis/*drug therapy/*metabolism",
author = "Felicitas M{\"u}ller and David Gailani and Thomas Renn{\'e}",
year = "2011",
language = "English",
volume = "18",
pages = "349--355",
journal = "CURR OPIN HEMATOL",
issn = "1065-6251",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

RIS

TY - JOUR

T1 - Factor XI and XII as antithrombotic targets.

AU - Müller, Felicitas

AU - Gailani, David

AU - Renné, Thomas

PY - 2011

Y1 - 2011

N2 - Arterial and venous thrombosis are major causes of morbidity and mortality, and the incidence of thromboembolic diseases increases as a population ages. Thrombi are formed by activated platelets and fibrin. The latter is a product of the plasma coagulation system. Currently available anticoagulants such as heparins, vitamin K antagonists and inhibitors of thrombin or factor Xa target enzymes of the coagulation cascade that are critical for fibrin formation. However, fibrin is also necessary for terminating blood loss at sites of vascular injury. As a result, anticoagulants currently in clinical use increase the risk of bleeding, partially offsetting the benefits of reduced thrombosis. This review focuses on new targets for anticoagulation that are associated with minimal or no therapy-associated increased bleeding.

AB - Arterial and venous thrombosis are major causes of morbidity and mortality, and the incidence of thromboembolic diseases increases as a population ages. Thrombi are formed by activated platelets and fibrin. The latter is a product of the plasma coagulation system. Currently available anticoagulants such as heparins, vitamin K antagonists and inhibitors of thrombin or factor Xa target enzymes of the coagulation cascade that are critical for fibrin formation. However, fibrin is also necessary for terminating blood loss at sites of vascular injury. As a result, anticoagulants currently in clinical use increase the risk of bleeding, partially offsetting the benefits of reduced thrombosis. This review focuses on new targets for anticoagulation that are associated with minimal or no therapy-associated increased bleeding.

KW - Animals

KW - Humans

KW - Anticoagulants/pharmacology/therapeutic use

KW - Blood Coagulation/drug effects/physiology

KW - Factor XI/antagonists & inhibitors/metabolism

KW - Factor XI Deficiency/blood/drug therapy/metabolism

KW - Factor XII/antagonists & inhibitors/metabolism

KW - Factor XII Deficiency/blood/drug therapy/metabolism

KW - Hemostasis/drug effects/physiology

KW - Thrombosis/drug therapy/metabolism

KW - Animals

KW - Humans

KW - Anticoagulants/pharmacology/therapeutic use

KW - Blood Coagulation/drug effects/physiology

KW - Factor XI/antagonists & inhibitors/metabolism

KW - Factor XI Deficiency/blood/drug therapy/metabolism

KW - Factor XII/antagonists & inhibitors/metabolism

KW - Factor XII Deficiency/blood/drug therapy/metabolism

KW - Hemostasis/drug effects/physiology

KW - Thrombosis/drug therapy/metabolism

M3 - SCORING: Journal article

VL - 18

SP - 349

EP - 355

JO - CURR OPIN HEMATOL

JF - CURR OPIN HEMATOL

SN - 1065-6251

IS - 5

M1 - 5

ER -