[Sarcoplasmic reticulum function and heart failure: a novel therapeutic target for heart failure]

Periodic changes in calcium (Ca(2+)) concentration in cardiomyocytes are essential for cardiac contraction and relaxation, and the intracellular Ca(2+)concentration is integrally regulated by proteins associated with the sarcoplasmic reticulum (SR), an extensive intracellular membrane system. The activity of the cardiac ryanodine receptor (RyR2) and the sarco/endoplasmic reticulum Ca(2+) ATPase 2a (SERCA2a) are known to be under fine-tuning by their intrinsic regulatory domains and associated SR proteins. A growing body of evidence, including studies using genetically engineered mouse models, has shown that Ca(2+)cycling and Ca(2+)-dependent signaling pathways play a pivotal role in heart failure. The improvement of the SR function has ameliorated effects on cardiac pump function and it has potential therapeutic value for heart failure.