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Factor V Leiden: a disorder of factor V anticoagulant function
Elisabetta Castoldi1, Jan Rosing
1Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, 6200 MD Maastricht, The Netherlands.
Current Opinion in Hematology
|July 17, 2004
Summary
Activated protein C (APC) resistance, linked to Factor V Leiden mutation, increases thrombosis risk. Impaired APC-cofactor activity of Factor V (FV) contributes to this risk, highlighting potential drug targets.
Area of Science:
- Hematology
- Molecular Biology
- Thrombosis Research
Background:
- Activated protein C (APC) resistance is a significant risk factor for venous thrombosis.
- The Factor V R506Q (FV Leiden) mutation is a common cause of APC resistance.
- Coagulation Factor V (FV) plays a crucial role in regulating blood clotting.
Purpose of the Study:
- To review the discovery and physiological significance of the APC-cofactor activity of FV.
- To explore the structural requirements for FV's APC-cofactor function.
- To understand how FV Leiden impacts APC resistance and thrombosis risk.
Main Methods:
- Review of in vitro and in vivo experimental data.
- Analysis of structural and functional aspects of FV.
- Correlation of FV defects with thrombosis risk.
Main Results:
- The anticoagulant activity of FV is physiologically relevant, maintaining hemostatic balance.
- Defects in FV's APC-cofactor activity elevate thrombin generation, leading to a prothrombotic state.
- While structural requirements are emerging, the molecular mechanism of FV's APC-cofactor activity remains unclear.
Conclusions:
- Impaired APC-cofactor activity in FV Leiden explains varying thrombosis risks.
- Understanding FV's anticoagulant mechanism may lead to new antithrombotic therapies.