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• W2036655503 abstract "Blood coagulation is thought to be initiated by plasma protease factor VIIa in complex with the membrane protein tissue factor. In contrast, coagulation factor XII (FXII)-mediated fibrin formation is not believed to play an important role for coagulation in vivo. We used FXII-deficient mice to study the contributions of FXII to thrombus formation in vivo. Intravital fluorescence microscopy and blood flow measurements in three distinct arterial beds revealed a severe defect in the formation and stabilization of platelet-rich occlusive thrombi. Although FXII-deficient mice do not experience spontaneous or excessive injury-related bleeding, they are protected against collagen- and epinephrine-induced thromboembolism. Infusion of human FXII into FXII-null mice restored injury-induced thrombus formation. These unexpected findings change the long-standing concept that the FXII-induced intrinsic coagulation pathway is not important for clotting in vivo. The results establish FXII as essential for thrombus formation, and identify FXII as a novel target for antithrombotic therapy." @default.
• W2036655503 created "2016-06-24" @default.
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• W2036655503 date "2005-07-11" @default.
• W2036655503 modified "2023-10-16" @default.
• W2036655503 title "Defective thrombus formation in mice lacking coagulation factor XII" @default.
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• W2036655503 doi "https://doi.org/10.1084/jem.20050664" @default.
• W2036655503 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2213000" @default.
• W2036655503 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16009717" @default.
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