Abstract
Introduction: Doxorubicin (Dox.) is a very effective antineoplastic agent for treating various tumours. It produces an anti-cancer mechanism through the intercalation of DNA and reducing topoisomerase II enzyme activity in fast-proliferating cancers. However, Dox. is associated with limited-use adverse effects specifically accumulative and dose-dependent heart toxicity which is the underlying cause for increasing the risk of mortality in cancer patients that use this kind of anticancer. Results: Many related mechanisms have been suggested for Dox.-induced cardiac toxicity such as oxidative stress and deteriorated mitochondrial function, a disturbance in iron regulatory protein [(IRP)-1], the release of nitric oxide, autophagy and dysregulation of Ca2+ level. Unfortunately, there is no clinically approved protective agent against Dox.-induced cardiotoxicity has been discovered yet. Aim: The current review attempts to focus on collecting information related to the mechanism of stimulating heart disease resulting from the use of Dox. and trying to understand it at the molecular level and addressing the most important compounds, especially the natural ones, and their proposed mechanism of action against Dox.-induced heart toxicity. Conclusion: Dox. still one of the most effective anticancer medications. Due to its undesirable cardiotoxicity and the lack of effective preventative methods, Dox. uses could increase the risk of death and restrict its potential clinical applications. Many mechanisms have been implicated in Dox.-induced cardiac toxicity. Therefore, targeting this alteration using bee propolis has shown strong protective effects against the cardiotoxicity of Dox. and the decrease the death rate among patients suffering from cancer.
