Tackling reperfusion injury - a side effect of heart attack treatment

Role of CX3CR1 and T-lymphocytes in myocardial ischaemia/reperfusion injury

In the UK the standard treatment for heart attacks is angioplasty - a procedure to quickly open the blocked coronary artery. This has played a part in vastly improving the survival of patients who experience a heart attack. However, the abrupt restoration of blood flow to the heart - called reperfusion - can itself cause further damage, and an increasing number of people go on to develop heart failure in the long term. Professor Spyridopoulos and his team are investigating the phenomenon of reperfusion injury to understand how this damage could be prevented. The team have experimental evidence that points to a role of the immune system in reperfusion injury. They’ve seen that a type of immune cells – called effector memory lymphocytes – stick to and penetrate the blood vessel walls in the heart early in the reperfusion process. This can plug the small arteries that nourish the heart muscle and cause injury. Control of this process appears to rely on a protein called fractalkine. In this project, the researchers will further study the role of the fractalkine pathway. They will use mice genetically engineered to lack the fractalkine pathway in the lymphocytes to test whether it reduces injury to the heart after reperfusion. Their results could identify a new target for medicines to prevent reperfusion injury after heart attack treatments.