Switching on blood vessel regeneration after a heart attack

Investigating the regulation of MEF2-driven angiogenesis in the coronary vasculature

The growth of new blood vessels could help to repair the damage caused to the heart by a heart attack. But efforts to promote the growth of new blood vessels in the heart have been limited by a lack of understanding of the normal biological processes that control how blood vessels grow. Dr Sarah De Val’s team at the University of Oxford has identified a process in mice that is active in normal hearts but switched off in damaged hearts. It centres around a molecule called MEF2, which is involved in the sprouting of new blood vessels. In this project, the team aims to find out if switching on this process can improve blood vessel growth in mice after a heart attack. To do this, they are focusing on a group of molecules that they believe might control MEF2, called histone deacetylases (HDACs). HDACs are being investigated by many other researchers looking at a number of different diseases, which means there are already drugs available that block them. The Oxford team will first look at where HDACs are found in heart blood vessels. They will then test the HDAC-blocking drugs to see which ones switch on MEF2 in blood vessel cells. They hope to then assess if HDAC-blocking drugs can promote blood vessel growth in the hearts of mice after a heart attack. If this is successful, these drugs could potentially be used in the future to treat people following a heart attack to help them recover.