[Reverse remodeling of the intracellular Ca(2+)-homeostasis: new concepts of pathophysiology and therapy of heart failure].

Cardiac contraction is dependent on a rapid alteration of the intracellular Ca(2+) concentration, especially the Ca(2+) released during systole. In end-stage heart failure, cardiac contractility is depressed due to alterations in the structure and function of proteins or protein complexes. Over recent years, new insights have been obtained regarding the regulation of the intracellular Ca(2+) homeostasis and its pathophysiological alteration in end-stage heart failure. This review focuses on the mechanisms involved in the release of Ca(2+) from the sarcoplasmic reticulum (SR) during systole via the ryanodine receptors and the Ca(2+)-uptake into the SR by the sarcoplasmic reticulum Ca(2+)-ATPase (SERCA 2a). In addition, new therapeutic options will be introduced which may be of importance for the treatment of heart failure patients.