Chapter 10 - Autophagy Upregulation Reduces Doxorubicin-Induced Cardiotoxicity

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Cardiotoxicity induced by anthracycline chemotherapy has become a serious concern over the years since the discovery of this class of drugs. These drugs are considered the most efficient, and are currently the most extensively used, anticancer agents for the treatment of numerous forms of cancer. The clinical utility of anthracycline drugs, however, is limited due to their cumulative, dose-dependent myocardial damage, which often results in irreversible alterations to the myocardium. Despite several decades of rigorous research, the molecular mechanisms that govern this event remain a matter of controversy. The emphasis on the role of oxidative stress, which induces oxidative damage to the myocardium, has been the main research focal point; but surely this oxidative stress hypothesis cannot be responsible for all the detrimental effects that have since been observed. At any rate, the time has arrived that we move away from this theory as it has currently been challenged after several unsuccessful antioxidant-based trials, and, rather, target cellular mechanisms that could be of potential benefit if exploited. One of the best understood and most widely studied processes is autophagy, an evolutionarily conserved pathway of intracellular degradation. Although it has been related to various cardiac disorders, an increasing body of evidence corroborates the notion of autophagy as a probable therapeutic target in providing a powerful cardioprotective treatment regimen.

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