Molecular mechanisms of doxorubicin-induced cardiotoxicity based on mitochondrial function and traditional Chinese medicine treatment

Abstract

<p indent="0mm">Doxorubicin (DOX), an anthracycline chemotherapeutic drug, is one of the most effective drugs for the treatment of various cancers. However, its therapeutic effect is seriously limited by related cardiotoxicity. Although this field has yielded many studies, the exact molecular mechanism of DOX-induced cardiotoxicity (DIC) is still worthy of further study. DOX is a mitochondrial toxin, and mitochondrial damage is the core of DIC. This paper reviews a large amount of literature and summarizes the mechanisms related to DIC that depend on mitochondrial dysfunction, including the effects of DOX on mitochondrial electron transport chain, redox cycle, oxidative stress, calcium imbalance, apoptosis pathway and mitophagy. In addition, it discusses the existing strategies of traditional Chinese medicine based on mitochondrial function to prevent and/or reduce DIC, to provide a scientific basis for combination of DOX and traditional Chinese medicine in the treatment of cancer.