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Editorial
. 2013 Jul;33(7):1454-5.
doi: 10.1161/ATVBAHA.113.301598.

Targeting factor XI to prevent thrombosis

Editorial

Targeting factor XI to prevent thrombosis

James H Morrissey. Arterioscler Thromb Vasc Biol. 2013 Jul.
No abstract available

Keywords: animal models; antisense oligonucleotides; factor XI; thrombosis.

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Figures

Figure
Figure
The revised plasma clotting cascade. In normal hemostasis, clotting is triggered at two points by the TF:VIIa pathway, leading first to activation of factors IX and X, and ultimately, thrombin generation and the formation of a fibrin clot. Thrombin also activates factor XI in a feedback reaction, that is greatly stimulated by platelet polyphosphate, which may be the physiologic cofactor for this reaction. Although factor XIIa is dispensable for normal hemostasis, it is a potent factor XI activator and a number of animal studies have shown that factor XII contributes to thrombosis. An open question, therefore, is what is the major pathway for factor XI activation in thrombotic diseases—activation by thrombin, factor XIIa, or perhaps both? (Not shown: factor XI can undergo autoactivation, which is also stimulated by polyphosphate.)

Comment on

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