Regulation of P2Y12 receptor expression and activity by inhibitory pathways in human platelets: A novel mode of action of antiplatelet drugs?
Heart attacks occur when blood flow is blocked, usually by a blood clot developing in the blood vessels of the heart. Platelets are the major cells involved in the formation of blood clots and can be ‘switched on’ by substances inside the body to become sticky and clump together. Being able to prevent this is an important approach to preventing and treating blood clotting and, therefore, heart attacks. Scientists have discovered that a molecule called P2Y12 is involved in this process. Switching P2Y12 on increases platelet stickiness, whereas blocking it has the reverse effect. This makes P2Y12 a potential target molecule for new treatments to prevent heart attacks. Dr Stuart Mundell and colleagues at the University of Bristol have shown that a molecule called prostacyclin, which is released by blood vessels, can switch off P2Y12 on human platelets. It’s thought that prostacyclin acts in the same way as an antiplatelet drug that is widely used to treat people with blood clots. In this project, Dr Mundell hopes to reveal exactly how prostacyclin and these antiplatelet drugs reduce P2Y12 function and prevent platelets being switched on. The results could lead to the development of more effective and safer drugs for the treatment and prevention of heart attacks.
Project details
| Grant amount | £219,235 |
|---|---|
| Grant type | Project Grants |
| Application type | Project Grant |
| Start Date | 02 July 2018 |
| Duration | 3 years |
| Reference | PG/17/62/33190 |
| Status | In Progress |
