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Comparative Study
. 2006 Mar 20;203(3):493-5.
doi: 10.1084/jem.20060217. Epub 2006 Mar 13.

Are hemostasis and thrombosis two sides of the same coin?

Robert W Colman  1
Affiliations
Comparative Study

Are hemostasis and thrombosis two sides of the same coin?

Robert W Colman. J Exp Med. .

Abstract

Factor XII (FXII), a clotting enzyme that can initiate coagulation in vitro, has long been considered dispensable for normal blood clotting in vivo because hereditary deficiencies in FXII are not associated with spontaneous or excessive bleeding. However, new studies show that mice lacking FXII are protected against arterial thrombosis (obstructive clot formation) and stroke. Thus, FXII could be a unique drug target that could be blocked to prevent thrombosis without the side effect of increased bleeding.

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Figures

Figure 1.
Figure 1.
Physiological coagulation. The extrinsic pathway is initiated by the binding of FVII to TF which results in the autoactivation of FVII (FVIIa). The activation of this pathway ultimately leads to the formation of thrombin, which feeds back to activate FXI on the surface of platelets. FXIa then triggers the intrinsic pathway generating more thrombin and accelerating fibrin formation.
Figure 2.
Figure 2.
Pathological thrombosis FXII is activated by exposure to negatively charged molecules to factor XIIa (FXIIa). FXIIa then cleaves FXI to FXIa, thus triggering the intrinsic pathway. Factor XIIa also hydrolyzes FVII to FVIIa, which combines with TF on the surface of activated monocytes or vascular cells to initiate the extrinsic system. Both coagulation pathways are required for pathological thrombosis as occurs during stroke and disseminated intravascular coagulation.
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Comment on

References

    1. Kleinschnitz, C., G. Stoll, M. Bendszus, K. Schuh, H.-U. Pauer, P. Burfeind, C. Renné, D. Gailani, B. Nieswandt, and T. Renné. 2006. Targeting coagulation factor XII provides protection from pathological thrombosis in cerebral ischemia without interfering with hemostasis. J. Exp. Med. 203:513–518. - PMC - PubMed
    1. Mackman, N. 2004. Role of tissue factor in hemostasis, thrombosis, and vascular development. Arterioscler. Thromb. Vasc. Biol. 24:1015–1022. - PubMed
    1. Osterud, B., and S.I. Rapaport. 1977. Activation of factor IX by the reaction product of tissue factor and factor VII: additional pathway for initiating blood coagulation. Proc. Natl. Acad. Sci. USA. 74:5260–5264. - PMC - PubMed
    1. Gailani, D., and G.J. Broze Jr. 1991. factor XI activation in a revised model of blood coagulation. Science. 253:909–912. - PubMed
    1. Renne, T., M. Pozgajova, S. Gruner, K. Schuh, H.U. Pauer, P. Burfeind, D. Gailani, and B. Nieswandt. 2005. Defective thrombus formation in mice lacking coagulation factor XII. J. Exp. Med. 202:271–281. - PMC - PubMed

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