Physicians at the Ruhr University Bochum announced Wednesday that they discovered previously unknown mechanisms that regulate the elasticity of the giant protein titin and thus the stiffness of the heart muscle. The team led by Prof. Dr. Wolfgang Linke with colleagues from the U.S. and from Dusseldorf wrote the results in two articles in the magazines "Cell" and "Journal of Cell Biology", explaining why the heart after stress, such as a heart attack, permanently loses their pumping power. According to the first article, Titin, the largest protein in the human body, acts like a spring that stretches the muscle cell or slackens them and its spring region has certain protein units, the so-called immunoglobulin domains, which are strung like pearls on a string. Under stress conditions, for example in acute heart failure, the spring region is excessively stretched and the immunoglobulin domains unfold. As the unfolded immunoglobulin domains can not return to its original structure, this reduces the stiffness of the heart wall and titin can not play its part as a sensor of the mechanical stress of cardiomyocytes, which limits the pumping function of the heart. In the second work, Linke and his colleagues showed that the heart muscle cells also possess mechanisms to protect the elastic region of titin from stress effects. The researchers showed that small proteins at the unfolded titin area wander and prevent the "pearls" of the spring region to clump together, which works against the pathological change of titin's elasticity in heart attacks or chronic heart disease.