Professor Thomas Krieg

Cardiovascular Ischaemia/Reperfusion Injury

A heart attack occurs when a blood clot forms in a coronary artery depriving blood flow from a region of the heart, a condition termed ischaemia. Current therapy is to reopen the artery but blood flow is seldom restored before a significant amount of the heart muscle has died. Because lost heart muscle cannot be regenerated the patient is left with a weakened heart and heart failure often occurs.

Our research is directed toward identifying therapies that prevent cell death in ischaemic heart. We have found that both population of G-coupled adenosine receptors and activation of the nitric oxide-PKG pathway just before the restoration of blood flow (reperfusion) makes the heart very resistant to cell death.

Our current research is directed at understanding the complex signal transduction pathways involved. We study these pathways using a model mirroring the pathophysiological events during an acute heart attack where we measure tissue death after a standardised ischemic insult as an end-point. We can then use pharmacological tools to both trigger and block the protection at specific points in the given pathway.

Secondly, we study isolated heart muscle cells as well as isolated mitochondria where protection can be analysed with certain techniques and the chemical signals can be measured directly using protein chemistry.