Factor XI deficiency in animal models
Standard
Factor XI deficiency in animal models. / Renné, T; Oschatz, C; Seifert, S; Müller, F; Antovic, J; Karlman, M; Benz, P M.
In: J THROMB HAEMOST, Vol. 7 Suppl 1, 01.07.2009, p. 79-83.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - Factor XI deficiency in animal models
AU - Renné, T
AU - Oschatz, C
AU - Seifert, S
AU - Müller, F
AU - Antovic, J
AU - Karlman, M
AU - Benz, P M
PY - 2009/7/1
Y1 - 2009/7/1
N2 - The blood coagulation system forms fibrin to limit blood loss from sites of injury, but also contributes to occlusive diseases such as deep vein thrombosis, myocardial infarction, and stroke. In the current model of a coagulation balance, normal hemostasis and thrombosis represent two sides of the same coin; however, data from coagulation factor XI-deficient animal models have challenged this dogma. Gene targeting of factor XI, a serine protease of the intrinsic pathway of coagulation, severely impairs arterial thrombus formation but is not associated with excessive bleeding. Mechanistically, factor XI may be activated by factor XII following contact activation or by thrombin in a feedback activation loop. This review focuses on the role of factor XI, and its deficiency states as novel target for prevention of thrombosis with low bleeding risk in animal models.
AB - The blood coagulation system forms fibrin to limit blood loss from sites of injury, but also contributes to occlusive diseases such as deep vein thrombosis, myocardial infarction, and stroke. In the current model of a coagulation balance, normal hemostasis and thrombosis represent two sides of the same coin; however, data from coagulation factor XI-deficient animal models have challenged this dogma. Gene targeting of factor XI, a serine protease of the intrinsic pathway of coagulation, severely impairs arterial thrombus formation but is not associated with excessive bleeding. Mechanistically, factor XI may be activated by factor XII following contact activation or by thrombin in a feedback activation loop. This review focuses on the role of factor XI, and its deficiency states as novel target for prevention of thrombosis with low bleeding risk in animal models.
KW - Animals
KW - Disease Models, Animal
KW - Factor XI Deficiency
KW - Hemorrhage
KW - Hemostasis
KW - Thrombosis
U2 - 10.1111/j.1538-7836.2009.03393.x
DO - 10.1111/j.1538-7836.2009.03393.x
M3 - SCORING: Journal article
C2 - 19630774
VL - 7 Suppl 1
SP - 79
EP - 83
JO - J THROMB HAEMOST
JF - J THROMB HAEMOST
SN - 1538-7933
ER -