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Factor XI deficiency in animal models.

T Renné1, C Oschatz, S Seifert

  • 1Department of Molecular Medicine and Surgery, Karolinska Institute, Karolinska University Hospital Solna, Stockholm, Sweden. thomas@renne.net

Journal of Thrombosis and Haemostasis : JTH
|July 28, 2009
PubMed
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Targeting factor XI, a key protein in blood clotting, may prevent dangerous clots like stroke and heart attack without increasing bleeding risk. Research in animal models shows factor XI deficiency hinders clot formation effectively.

Area of Science:

  • Biochemistry
  • Hematology
  • Vascular Biology

Background:

  • The blood coagulation system is crucial for hemostasis but also implicated in thrombotic diseases like DVT, MI, and stroke.
  • The traditional coagulation balance model views hemostasis and thrombosis as interconnected.
  • Emerging data challenges this dogma, particularly from studies on factor XI deficiency.

Purpose of the Study:

  • To review the role of coagulation factor XI in thrombosis and hemostasis.
  • To explore factor XI deficiency as a potential therapeutic target for preventing thrombosis.
  • To evaluate the associated bleeding risk in factor XI-deficient models.

Main Methods:

  • Review of existing literature on coagulation factor XI.
  • Analysis of data from genetically modified animal models with factor XI deficiency.

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  • Examination of the mechanisms of factor XI activation.

    • Main Results:

    • Factor XI deficiency significantly impairs arterial thrombus formation in animal models.
    • Factor XI deficiency is not associated with excessive bleeding complications.
    • Factor XI activation can occur via contact activation (factor XII) or thrombin feedback loops.

    Conclusions:

    • Factor XI plays a critical role in pathological thrombosis.
    • Targeting factor XI offers a promising strategy for antithrombotic therapy with a potentially low bleeding risk.
    • Factor XI deficiency in animal models supports its role as a novel therapeutic target.