Research Papers: Pathology:
CaMKII inhibition reduces isoproterenol-induced ischemia and arrhythmias in hypertrophic mice
Metrics: PDF 2067 views | HTML 2113 views | ?
Ying Feng1,*, Jun Cheng1,*, Baozhu Wei1 and Yanggan Wang1,2
1 Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan, China
2 The Medical Research Institute of Wuhan University, Wuhan, China
* These authors have contributed equally to this work
Yanggan Wang, email:
Keywords: arrhythmia; CaMKII; cardiac hypertrophy; adrenergic stimulation; Pathology Section
Received: August 04, 2016 Accepted: January 23, 2017 Published: February 04, 2017
Objectives: The Ca/calmodulin-dependent protein kinase II (CaMKII), an arrhythmogenic molecule, is excessively activated in cardiac hypertrophy. Here, we investigated the effect of CaMKII inhibition in isoproterenol (ISO)-induced arrhythmias in hypertrophic mice.
Results: ISO induced multiple types of arrhythmias in the hypertrophic mice but not in the normal mice. The QTc intervals were prolonged and the amplitudes of T waves were increased significantly by ISO prior to arrhythmia initiation. Inhibition of CaMKII prevented ISO-induced QTc prolongation and T wave elevation and abrogated arrhythmia induction.
Materials and Methods: Pressure-overload cardiac hypertrophy was induced in mice by thoracic aortic banding. Arrhythmias were recorded by electrocardiogram in conscious mice.
Conclusions: CaMKII inhibition is effective in suppressing adrenergic activation-induced ventricular arrhythmias in cardiac hypertrophy, of which the ventricular ischemia-induced CaMKII activation plays an important role.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.