Oxidized CaMKII (Ca2+/Calmodulin-Dependent Protein Kinase II) Is Essential for Ventricular Arrhythmia in a Mouse Model of Duchenne Muscular Dystrophy [Original Articles]
Conclusions:
Inhibition of reactive oxygen species or ox-CaMKII protects against proarrhythmic intracellular Ca2+ handling and prevents ventricular arrhythmia in a mouse model of Duchenne muscular dystrophy.
Source: Circulation: Arrhythmia and Electrophysiology - Category: Cardiology Authors: Wang, Q., Quick, A. P., Cao, S., Reynolds, J., Chiang, D. Y., Beavers, D., Li, N., Wang, G., Rodney, G. G., Anderson, M. E., Wehrens, X. H. T. Tags: Arrhythmias, Animal Models of Human Disease, Cell Signaling/Signal Transduction, Oxidant Stress, Cardiomyopathy Original Articles Source Type: research
More News: Arrhythmia | Calcium | Cardiology | Cardiomyopathy | Genetics | Heart | Muscular Dystrophy | Reflex Sympathetic Dystrophy | Study | Ventricular Arrhythmia | Ventricular Tachycardia