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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Authors | Robert W Colman |
Journal | The Journal of experimental medicine
(J Exp Med)
Vol. 203
Issue 3
Pg. 493-5
(Mar 20 2006)
ISSN: 0022-1007 [Print] United States |
PMID | 16533890
(Publication Type: Comment, Comparative Study, Journal Article)
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Chemical References |
- Blood Coagulation Factor Inhibitors
- Factor XII
- Fibrin
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Topics |
- Animals
- Blood Coagulation Factor Inhibitors
(administration & dosage)
- Blood Vessels
(metabolism, pathology)
- Brain Ischemia
(drug therapy, metabolism, pathology)
- Factor XI Deficiency
(drug therapy, metabolism, pathology)
- Factor XII
(antagonists & inhibitors, metabolism)
- Factor XII Deficiency
(metabolism, pathology)
- Female
- Fibrin
(metabolism)
- Hemostasis
(drug effects)
- Male
- Mice
- Mice, Knockout
- Thrombosis
(drug therapy, metabolism, pathology)
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