Alliance for Calmodulin Kinase II Signaling in Heart Failure and Arrhythmias
- Silvia G. PRIORI, University of Pavia (Italy)
- Mark E. ANDERSON, University of Iowa, Iowa City (USA)
- Michael J. ACKERMAN, Mayo Clinic College of Medicine, Rochester (USA)
- Donald M. BERS, University of California, Davis (USA)
- Karin R. SIPIDO, University of Leuven (Belgium)
- Marc A. VOS, University of Utrecht (The Netherlands)
- J. Kevin DONAHUE, Case Western Reserve University, Cleveland (USA)
- Albert J. HECK, University of Utrecht (The Netherlands)
- Lars S. MAIER, University Medical Center Göttingen (Germany)
- Peter J. MOHLER, Ohio State University, Columbus (USA)
- Carlo NAPOLITANO, IRCCS Fondzione S. Maugeri, Pavia (Italy)
- Steven M. POGWIZD, University of Alabama, Birmingham (USA)
- Yoram RUDY, Washington University School of Medicine, Saint Louis (USA)
- Xander H. WEHRENS, Baylor College of Medicine, Houston (USA)
Heart failure remains one of the leading sources of mortality and morbidity worldwide, despite a significant research effort at the international level. Much has been learned about what happens in heart failure at the molecular level, yet the perturbations of signaling, metabolism, and genetic regulation are complex and remain largely obscure. This network focuses on a signaling pathway involving calmodulin-dependent protein kinase II (CaMKII), which appears to act as a kind of master switch to activate pathways leading to arrhythmia and heart failure. This research may help to explain the increased propensity to arrhythmia found in patients in heart disease. Should CaMKII prove crucial to the development of heart failure, network members will look into therapeutic interventions targeted at inhibiting CaMKII, with the hope to provide more effective treatment for patients with heart failure.