A role for calcium/calmodulin-dependent protein kinase II in cardiac disease and arrhythmia

• Published in: Handbook of experimental pharmacology no. 171; p. 201
• Main Authors: Hund, T J, Rudy, Y
• Format: Journal Article
• Language: English
• Published: Germany 2006
• Subjects: Animals; Arrhythmias, Cardiac - etiology; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Calcium-Calmodulin-Dependent Protein Kinases - chemistry; Calcium-Calmodulin-Dependent Protein Kinases - physiology; Cardiomegaly - etiology; Heart Failure - etiology; Humans; Ischemic Preconditioning, Myocardial; Myocardial Reperfusion Injury - etiology; Myocytes, Cardiac - enzymology; Myocytes, Cardiac - physiology
• ISSN: 0171-2004
• DOI: 10.1007/3-540-29715-4_7

More than 20 years have passed since the discovery that a collection of specific calcium/calmodulin-dependent phosphorylation events is the result of a single multifunctional kinase. Since that time, we have learned a great deal about this multifunctional and ubiquitous kinase, known today as calcium/calmodulin-dependent protein kinase II (CaMKII). CaMKII is interesting not only for its widespread distribution and broad specificity but also for its biophysical properties, most notably its activation by the critical second messenger complex calcium/calmodulin and its autophosphorylating capability. A central role for CaMKII has been identified in regulating a diverse array of fundamental cellular activities. Furthermore, altered CaMKII activity profoundly impacts function in the brain and heart. Recent findings that CaMKII expression in the heart changes during hypertrophy, heart failure, myocardial ischemia, and infarction suggest that CaMKII may be a viable therapeutic target for patients suffering from common forms of heart disease.