The research team, led by Professor Jon Gibbins from the University’s Institute for Cardiovascular and Metabolic Research (ICMR), found that rosiglitazone¹ inhibits blood clot formation by 50%.
Professor Gibbins and his team have discovered that rosiglitazone, used to treat type 2 diabetes (the type caused by obesity), also inhibits platelet function – thereby preventing thrombosis. Crucially, the team have made substantial progress on understanding how this works, paving the way towards the development of new therapies to prevent thrombosis.
Platelets are tiny blood cells that trigger the blood to clot when the blood vessel is damaged, a normal protective function that prevents excessive blood loss. In diseased blood vessels (such as those associated with obesity, diabetes and coronary artery disease) this triggers thrombosis, the formation of blood clots within the circulation. Thrombosis leads to heart attacks and strokes which together are the leading causes of death in the western world.
Professor Gibbins said: “We already know that patients treated using these types of medicines experience a reduced risk of suffering from cardiovascular problems, but we now have a clearer idea why. Rosiglitazone acts on a target molecule, which we have found to be present in platelets, and suppresses their function. This suppression makes the platelets less active and so reduces the blood clotting response. We hope that this may lead to new therapies to prevent the occurrence of heart attacks and strokes.”
Cardiovascular diseases, which include heart attacks, strokes and heart failure, are the cause of approximately 190,000 deaths each year in the UK alone. Professor Gibbins has been examining the role of blood cells in blood clotting and thrombosis, which cause heart attacks and strokes
Earlier this year, Professor Gibbins and his team were awarded almost £1 million pounds by the British Heart Foundation, to continue their cutting-edge research exploring new and better ways to prevent heart attacks and strokes.
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Notes for Editors:
¹ Tested at levels comparable to blood concentrations following rosiglitazone administration (1 µmol L-1) and under arterial flow conditions
This work was supported by research grants from Heart Research UK, British Heart Foundation and The Wellcome Trust.
The paper has been accepted online but not yet been published in print. A pdf of the paper is available upon request.
Moraes, L. A. et al. 2009. Non-genomic effects of PPARg ligands: inhibition of GPVI-stimulated platelet activation. Journal of Thrombosis and Haemostasis. 8:1-11
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