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Heart failure is the leading cause of mortality in the world, responsible for at least 20 per cent of all hospital admissions among people over 65 in the United States. What causes the loss of heart muscles cells associated with heart failure and ischemic heart disease has been unclear. Now, researchers and clinicians in Germany have demonstrated for the first time that heart failure is triggered by apoptosis, a programm which causes the heart muscle cells to commit suicide. They also showed that a survival factor, abbreviated ARC, is able to protect the heart. The findings of Dr. Stefan Donath, Dr. Peifing Li, Prof. Rainer Dietz, and Dr. Rüdiger von Harsdorf (now Toronto, Canada) from the Charité - Medical School of the University of Berlin and the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch have now been published in the journal Circulation (2006; 113:1203-1212)*.
Usually apoptosis or programmed cell death protects the organism by ridding it of those cells that are ill or have lost their function. Cancer researchers aim to use this innate programme for cancer therapy, artificially activating apoptosis in cancer cells which have lost this function and, therefore, continue to grow indefinitely. Contrary to cancer cells which do not die off as part of a natural process, in heart failure, heart muscle cells are increasingly lost due to apoptosis, as demonstrated by the researchers. Despite drug therapy, patients with heart failure have a poor prognosis.
The researchers also looked closer at a factor, termed apoptosis repressor with caspase recruitment domain (ARC), which was previously detected and is present only in heart muscle cells and nerve cells. In laboratory mice, the scientists turned off the ARC gene and noted that they appeared healthy while resting. However, as soon as the mice were under physical stress, they experienced heart failure. The researchers could also demonstrate that those patients who had suffered from heart failure and, thereafter, received a heart transplant have significantly reduced ARC protein levels when compared to healthy individuals. This probably makes ARC an interesting target for future therapy, Dr. Donath postulates. The scientists and clinicians whose work is supported by the German Heart Failure Network will now investigate the role of ARC in nerve cells and stroke. This research could potentially lead to new and effective therapies for these diseases.
*Apoptosis Repressor With Caspase Recruitment Domain Is Required for Cardioprotection in Response to Biomechanical and Ischemic Stress
Stefan Donath, Peifeng Li, Christian Willenbockel, Nidal Al-Saadi, Volkmar Gross, Thomas Willnow, Michael Bader, Ulrich Martin, Johann Bauersachs, Kai C. Wollert, Rainer Dietz, Rüdiger von Harsdorf on behalf of the German Heart Failure Network
From the Departments of Cardiology, Campus Virchow Clinic, Charité, Humboldt University, and Franz-Volhard Clinic, HELIOS GmbH, Berlin, Germany (S.D., P.L., N.A., R.D., R.v.H.); Max Delbrück Center for Molecular Medicine, Berlin, Germany (S.D., V.G., T.W., M.B., R.v.H.); Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany (C.W., K.C.W.); Leibniz Research Laboratories for Biotechnology and Artificial Organs, Department of Thoracic and Cardiovascular Surgery, Hannover Medical School, Hannover, Germany (U.M.); and Department of Internal Medicine I, Julius-Maximilians University, Würzburg, Germany (J.B.).
*The first 2 authors contributed equally to this work.
Correspondence to Rüdiger von Harsdorf, MD, FRCPS, Associate Professor of Medicine, Division of Cardiology, University
Health Network, 200 Elizabeth St, MaRS 3-908, Toronto, ON, M5G 2C4, Canada. E-mail rudiger.vonharsdorf@uhn.on.ca
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Max Delbrück Center for Molecular Medicine(MDC) Berlin-Buch
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e-mail: bachtler@mdc-berlin.de
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