Abstract | PURPOSE OF REVIEW: Blood coagulation is a tightly regulated process, involving vascular endothelium, platelets, and plasma coagulation factors. Formation of fibrin involves a series of sequential proteolytic reactions, initiated by the 'extrinsic' and 'intrinsic' pathway of coagulation. As hereditary deficiency of factor XII, the protease that triggers the intrinsic pathway and the kallikrein-kinin system, is not associated with a bleeding disorder or other disease states, the physiological role of factor XII is unknown. RECENT FINDINGS: SUMMARY: Recent studies improved understanding of the factor XII-driven contact system in hemostasis, thrombosis, and inflammation. Studies in mouse models revealed that deficiency in contact system proteins protects from arterial thrombus formation, but does not affect hemostasis. Targeting contact system proteins offers new opportunities for safe anticoagulation associated with minimal bleeding risk. Furthermore, targeting factor XII activity provides an opportunity to treat edema formation.
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Authors | Felicitas Müller, Thomas Renné |
Journal | Current opinion in hematology
(Curr Opin Hematol)
Vol. 15
Issue 5
Pg. 516-21
(Sep 2008)
ISSN: 1531-7048 [Electronic] United States |
PMID | 18695377
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
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Topics |
- Animals
- Blood Coagulation
- Factor XII
(metabolism, physiology)
- Hemostasis
- Humans
- Inflammation
- Protein Binding
- Thrombosis
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