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Abstract
Factor XII (FXII) is a coagulation protein that is essential for surface-activated
blood coagulation tests but whose deficiency is not associated with bleeding. For
over forty years, investigators in hemostasis have not considered FXII important because
its deficiency is not associated with bleeding. It is because there is a dichotomy
between abnormal laboratory assay findings due to FXII deficiency and clinical hemostasis
that investigators sought explanations for physiologic hemostasis independent of FXII.
FXII is a multidomain protein that contains two fibronectin binding consensual sequences,
two epidermal growth factor regions, a kringle region, a proline-rich domain, and
a catalytic domain that when proteolyzed turns into a plasma serine protease. Recent
investigations with FXII deleted mice that are protected from thrombosis indicate
that it contributes to the extent of developing thrombus in the intravascular compartment.
These findings suggest that it has a role in thrombus formation without influencing
hemostasis. Last, FXII has been newly appreciated to be a growth factor that may influence
tissue injury repair and angiogenesis. These combined studies suggest that FXII may
become a pharmacologic target to reduce arterial thrombosis risk and promote cell
repair after injury, without influencing hemostasis.
(c) 2009 Elsevier Ltd. All rights reserved.