Oxidized CaMKII (Ca²⁺/Calmodulin-Dependent Protein Kinase II) Is Essential for Ventricular Arrhythmia in a Mouse Model of Duchenne Muscular Dystrophy.

ABSTRACT:

Background

Duchenne muscular dystrophy patients are prone to ventricular arrhythmias, which may be caused by abnormal calcium (Ca²⁺) homeostasis and elevated reactive oxygen species. CaMKII (Ca²⁺/calmodulin-dependent protein kinase II) is vital for normal Ca²⁺ homeostasis, but excessive CaMKII activity contributes to abnormal Ca²⁺ homeostasis and arrhythmias in cardiomyocytes. Reactive oxygen species induce CaMKII to become autonomously active. We hypothesized that genetic inhibition of CaMKII oxidation (ox-CaMKII) in a mouse model of Duchenne muscular dystrophy can alleviate abnormal Ca²⁺ homeostasis, thus, preventing ventricular arrhythmia. The objective of this study was to test if selective loss of ox-CaMKII affects ventric

SUBMITTER: Wang Q 

PROVIDER: S-EPMC5903581 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature