Affiliations: Department of Haematology, Bristol Royal infirmary,
Bristol, BS2 8HW, UK | Haemostasis and Thrombosis, MRC Clinical Sciences
Centre, The Faculty of Medicine, Imperial College, Hammersmith Hospital Campus,
Du Cane Road, London, W12 0NN, UK
Note: [] Corresponding author: Dr. AD Mumford, Department of
Haematology, Bristol Royal infirmary, Bristol, BS2 8HW, UK. Tel.: +44 117 928
2655; Fax: +44 117 928 4036; E-mail: a.mumford@bristol.ac.uk
Abstract: The interaction between cell-surface tissue factor (TF) and the
plasma coagulation factor VII (FVII) initiates the coagulation network that
leads to the generation of thrombin and the formation of a fibrin clot.
Thrombin also activates cellular protease activated receptors (PARs) through
which it activates components of the inflammatory pathway. TF is expressed
constitutively by cardiomyocytes and evidence from mice transgenic for a human
TF mini-gene that express very low levels of human TF suggests that the TF-FVII
interaction is critical for haemostasis within the heart. Pathological contact
between TF and FVII may occur in the heart during ischaemia-reperfusion (I-R)
injury and this may lead to activation of coagulation and thrombin generation.
Evidence from animal models now suggests that thrombin is an important mediator
of inflammation in I-R injury. The coagulation pathway therefore represents a
novel therapeutic target for intervention in the prevention of I-R injury.
