Blood clots are the leading cause of death in Australia and are associated with stroke, deep vein thrombosis (DVT), pulmonary embolism (PE) and coronary heart disease. Approximately 30,000 Australians are hospitalised each year due to DVT and/or PE.

Haemostasis is the biological process that occurs in response to vascular trauma to prevent blood loss from the body. The blood coagulation pathway results from a cascade of protease activations occurring via separate pathways that merge together in a common pathway to form thrombin, a key player in the formation of the fibrin blood clot. Blood coagulation is controlled by anticoagulant pathways and the formed clots are dissolved by fibrinolysis in order to prevent deleterious thrombosis from occurring. In addition to circumstantial factors, both biochemical and genetic risk factors in the procoagulant, anticoagulant and fibrinolytic pathways can favour the predisposition of blood clotting and thrombosis. This complex process requires balanced interaction of the endothelium, platelets and proteins involved in procoagulant, anticoagulant and fibrinolytic pathways; if the balance is tipped in favour of coagulation, thrombosis may result.

The research interests of the lab are focused not only on the mechanisms of the biochemical or genetic risks on blood coagulation pathways but also investigate in a translational research setting how they associate with clinical conditions which show a thrombotic phenotype or excessive coagulopathy.