What causes the loss of heart muscle cells associated with heart failure and ischemic heart disease has been unclear so far. Now, researchers and clinicians in Germany have demonstrated for the first time that heart failure is triggered by apoptosis, a program which causes the heart muscle cells to commit suicide. They also showed that a survival factor, abbreviated ARC, is able to protect the heart.

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 for cancer therapy, artificially activating apoptosis in cancer cells which have lost this function. 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 will now investigate the role of ARC in nerve cells and stroke.
