CaMKII inhibition reduces isoproterenol-induced ischemia and arrhythmias in hypertrophic mice

Ying Feng; Jun Cheng; Baozhu Wei; Yanggan Wang

doi:10.18632/oncotarget.15099

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Research Papers: Pathology:

CaMKII inhibition reduces isoproterenol-induced ischemia and arrhythmias in hypertrophic mice

Ying Feng, Jun Cheng, Baozhu Wei and Yanggan Wang _

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Oncotarget. 2017; 8:17504-17509. https://doi.org/10.18632/oncotarget.15099

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Abstract

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

Correspondence to:

Yanggan Wang, email:

Keywords: arrhythmia; CaMKII; cardiac hypertrophy; adrenergic stimulation; Pathology Section

Received: August 04, 2016 Accepted: January 23, 2017 Published: February 04, 2017

Abstract

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.

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Research Papers: Pathology:

CaMKII inhibition reduces isoproterenol-induced ischemia and arrhythmias in hypertrophic mice

Abstract