Cardiac arrhythmias and antiarrhythmic drugs: An autophagic perspective

Abstract

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.