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: Tags: Arrhythmias, Animal Models of Human Disease, Cell Signaling/Signal Transduction, Oxidant Stress, Cardiomyopathy Original Articles Source Type: research

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More News: Arrhythmia | Calcium | Cardiology | Cardiomyopathy | Genetics | Heart | Muscular Dystrophy | Reflex Sympathetic Dystrophy | Study | Ventricular Arrhythmia | Ventricular Tachycardia