Heart attack research wins award

The European Society of Anaesthesiology (ESA) has awarded the 2012 ‘ESA Dräger Prize in Anaesthesia and Intensive Care Medicine’ to the research group headed by associate professor Dr Alexander Zarbock, department of anaesthesiology, intensive care and pain management, at the University Hospital of Münster, and Max Planck Institute for Molecular Biomedicine, Münster, Germany.

The scientists identified a protein occurring naturally in the body that is essential for the repair of the heart after a heart attack. After a heart attack, the body must replace dead heart muscle tissue with a stable scar. The working group led by Zarbock, together with a working group of the Medical School of Hannover, under the supervision of Professor Kai C. Wollert, observed that the heart muscle increases the body’s own protein GDF-15 during this process. They determined that GDF-15 plays a protective role in the breakdown of dead tissue – even in tissues outside the heart: in an inflammatory reaction, for example, after a heart attack, white blood cells migrate from the blood to the center of the inflammation. This requires that integrin molecules are activated on the surface of white blood cells. The researchers have now discovered for the first time that GDF-15 inhibits the activation of these integrins and thus ensures that the dead tissue is not broken down too quickly and that the inflammatory process takes place in a controlled manner. Dräger, a supplier of medical and safety technology, donated prize money of e10,000.


The scientists identified a protein occurring naturally in the body that is essential for the repair of the heart after a heart attack. After a heart attack, the body must replace dead heart muscle tissue with a stable scar. The working group led by Zarbock, together with a working group of the Medical School of Hannover, under the supervision of Professor Kai C. Wollert, observed that the heart muscle increases the body’s own protein GDF-15 during this process. They determined that GDF-15 plays a protective role in the breakdown of dead tissue – even in tissues outside the heart: in an inflammatory reaction, for example, after a heart attack, white blood cells migrate from the blood to the center of the inflammation. This requires that integrin molecules are activated on the surface of white blood cells. The researchers have now discovered for the first time that GDF-15 inhibits the activation of these integrins and thus ensures that the dead tissue is not broken down too quickly and that the inflammatory process takes place in a controlled manner. Dräger, a supplier of medical and safety technology, donated prize money of e10,000.



 

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