Impact Factor 4.134

The 2nd most cited  journal in Physiology

This article is part of the Research Topic

Ion Channel Trafficking and Cardiac Arrhythmias

Perspective ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Physiol. | doi: 10.3389/fphys.2018.00127

Cardiac arrhythmias and antiarrhythmic drugs: an autophagic perspective

  • 1Medical Physiology Division Heart & Lungs, University Medical Center Utrecht, Netherlands

Degradation of cellular material by lysosomes is known as autophagy, and its main function is to maintain cellular homeostasis for growth, proliferation and survival of the cell. In recent years, research has focused on the characterization of autophagy pathways. Targeting of autophagy mediators has been described predominantly in cancer treatment, but also in neurological and cardiovascular diseases. Although the number of studies is still limited, there are indications that activity of autophagy pathways increases under arrhythmic conditions. Moreover, an increasing number of antiarrhythmic and non-cardiac drugs are found to affect autophagy pathways. We, therefore, suggest that future work should recognize the largely unaddressed effects of antiarrhythmic agents and other classes of drugs on autophagy pathway activation and inhibition.

Keywords: Autophagy, AMPK, Antiarrhythmic drugs, arrhythmias, mTOR, Heart

Received: 24 Nov 2017; Accepted: 07 Feb 2018.

Edited by:

Carol Ann Remme, University of Amsterdam, Netherlands

Reviewed by:

Rob Gourdie, Medical University of South Carolina, United States
Craig Doupnik, Morsani College of Medicine, University of South Florida, United States
Thomas Hund, The Ohio State University, United States  

Copyright: © 2018 van Bavel, Vos and van der Heyden. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Marcel A. van der Heyden, University Medical Center Utrecht, Medical Physiology Division Heart & Lungs, Yalelaan 50, Utrecht, 3584 CM, Netherlands,