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.
Highlights
Degradation of cellular material occurs mainly via two pathways: the ubiquitin-proteasome system (UPS) and the autophagy-lysosome pathway
Evidence has brought forward that autophagy activation changes in arrhythmic conditions of the heart
Some antiarrhythmic drugs have been shown to affect autophagy pathways and this may associate with adverse effects
Summary
Degradation of cellular material occurs mainly via two pathways: the ubiquitin-proteasome system (UPS) and the autophagy-lysosome pathway. The UPS targets mainly short-lived or misfolded proteins, whereas autophagy includes the degradation, digestion and recycling of autophagy substrates, by lysosomes (Li et al, 2012). An increasing amount of research has focused on autophagy and attention has been paid to the association between autophagy and cardiac diseases, including ischemia and hypertrophy. A potential link between arrhythmic conditions and changes in autophagy activity has gained little attention, the evidence for such interaction currently expands. There remains a need for increased research focus on the association between pro- and antiarrhythmic drugs and autophagy pathways in the heart. We review the link between cardiac autophagy and arrhythmic conditions, and the limitations regarding the effect of antiarrhythmic drugs on autophagy. A few years we can determine whether the current niche of arrhythmias and autophagy research will emerge in a mature field of investigation
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