Autophagy and mitophagy in the context of doxorubicin-induced cardiotoxicity
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Navid Koleini1,2 and Elissavet Kardami1,2,3
1 Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, Winnipeg, Manitoba, Canada
2 Department of Physiology and Pathophysiology, Winnipeg, Manitoba, Canada
3 Department of Human Anatomy and Cell Sciences, University of Manitoba, Winnipeg, Manitoba, Canada
Elissavet Kardami, email:
Keywords: oncocardiology, anthracyclines, heart failure, impaired autophagy and mitophagy, lysosomal dysfunction
Received: November 25, 2016 Accepted: March 17, 2017 Published: April 07, 2017
Doxorubicin (Dox) is a cytotoxic drug widely incorporated in various chemotherapy protocols. Severe side effects such as cardiotoxicity, however, limit Dox application. Mechanisms by which Dox promotes cardiac damage and cardiomyocyte cell death have been investigated extensively, but a definitive picture has yet to emerge. Autophagy, regarded generally as a protective mechanism that maintains cell viability by recycling unwanted and damaged cellular constituents, is nevertheless subject to dysregulation having detrimental effects for the cell. Autophagic cell death has been described, and has been proposed to contribute to Dox-cardiotoxicity. Additionally, mitophagy, autophagic removal of damaged mitochondria, is affected by Dox in a manner contributing to toxicity. Here we will review Dox-induced cardiotoxicity and cell death in the broad context of the autophagy and mitophagy processes.
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