Investigating new ways to prevent thrombosis

GPVI-dimer, a specific target in ischaemic heart disease and stroke

Many types of heart and circulatory disease occur because of the build-up of dangerous ‘fatty’ plaques in the walls of blood vessels. During this process blood cells and fatty material become trapped in an area of the vessel wall. Some plaques become inflamed and unstable, and can rupture, triggering a blood clot. If a plaque ruptures and causes a blockage (thrombosis) in arteries supplying the heart or brain, a heart attack, or stroke, can occur. A key component of plaques and resultant clots is platelets. Platelets are tiny cells in the blood which, when active, become sticky and attach to injured blood vessel walls. Although this is an important healing response to bleeding, if a clot forms inside a vessel this can have a devastating effect. Dr Stephanie Jung and colleagues from the University of Cambridge are a team that specialise in looking at platelet behaviour. They have been awarded a four year project grant of nearly £800,000 to investigate how platelets attach to injured blood vessels. Their previous work has identified that platelets bind to blood vessels using a special protein on their surface called glycoprotein VI (GPVI). Now they will investigate if small molecules they are making in the lab can bind to GPVI, and stop platelets binding to blood vessels. This will hopefully help to reduce thrombosis. They will look at the effect of the small molecules on platelets obtained from healthy individuals and from patients with heart disease. They will also look to see whether high levels of GPVI puts someone at higher risk of heart attack or stroke, or increases the likelihood of these recurring. This exciting research could identify a new treatment for heart disease that works by preventing dangerous clot formation.