Abstract
The multifunctional Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) has emerged as a proarrhythmic and procardiomyopathic signal in a wide range of structural heart diseases. This review discusses CaMKII structure and function and recent evidence implicating CaMKII inhibition as a potential strategy for treating myocardial dysfunction and arrhythmias in the setting of structural heart disease.
Original language | English (US) |
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Pages (from-to) | 39-55 |
Number of pages | 17 |
Journal | Pharmacology and Therapeutics |
Volume | 106 |
Issue number | 1 |
DOIs | |
State | Published - Apr 2005 |
Externally published | Yes |
Keywords
- Arrhythmia
- Calmodulin kinase
- Cellular calcium
- Electrophysiology
- Structural heart disease
- Sudden death
ASJC Scopus subject areas
- Pharmacology
- Pharmacology (medical)