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The true colors of autophagy in doxorubicin-induced cardiotoxicity

机译:自噬在阿霉素诱导的心脏毒性中的本色

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摘要

Patients with cancer receiving doxorubicin-based chemotherapy often have to stop taking the drug due to its cardiotoxicity and therefore lose out on the beneficial effects of its potent antitumor activity. Doxorubicin has been demonstrated to damage cardiomyocytes via various mechanisms, including accumulation of reactive oxygen species (ROS), DNA damage and autophagy dysfunction. The present review focuses on autophagy, describing the general process of autophagy and the controversy surrounding its role in doxorubicin-induced cardiotoxicity. In addition, the associations between autophagy and apoptosis, ROS, DNA damage and inflammatory processes are discussed. In the future, it will be useful to further elucidate the process of autophagy and reveal its association with various pathological processes to develop effective strategies of preventing doxorubicin-induced cardiotoxicity.
机译:接受基于阿霉素的化学疗法的癌症患者由于其心脏毒性常常不得不停止服用该药物,因此会失去其有效抗肿瘤活性的有益作用。已证明阿霉素可通过多种机制破坏心肌细胞,包括活性氧(ROS)积累,DNA破坏和自噬功能障碍。本综述侧重于自噬,描述了自噬的一般过程以及围绕其在阿霉素诱导的心脏毒性中作用的争议。此外,讨论了自噬与细胞凋亡,ROS,DNA损伤和炎症过程之间的关系。将来,进一步阐明自噬过程并揭示其与各种病理过程的联系对于开发预防阿霉素诱导的心脏毒性的有效策略将很有用。

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