July 2015

Together with cell biologists from Saarland University, DZHK investigators at the Heidelberg-Mannheim partner site have discovered a mechanism involving calcium channel proteins that plays a key role in the development of chronic heart failure. Calcium is essential for maintaining cardiac function – very rapid, cyclic changes in the calcium levels in the heart cells keep the heartbeat going. The investigators had evidence that calcium is also involved in pathological remodelling of heart muscle cells under stress, as caused for instance by high blood pressure. They genetically modified mice so that both calcium channel proteins, TRPC1 and TRPC4, were switched off in the hearts of the animals. Despite having artificially induced high blood pressure or aortic narrowing, these animals had significantly reduced pathological heart muscle growth – they were protected from heart failure throughout the period of the study. Both proteins are therefore suitable starting points for new therapies to combat heart failure. The researchers now plan to develop drugs that inhibit TRPC1 and TRPC4.  

Link to the Paper