多柔比星（DOX）是一种广泛使用的化疗药物，可能引起严重且频繁的心脏毒性反应，限制了其临床应用。尽管关于DOX引起的心脏毒性已进行了大量的研究，但有效的治疗方法仍然缺乏。了解DOX诱导心脏毒性的分子机制，并寻找不会牺牲其抗癌效果的新的治疗靶点是必要的。线粒体被认为是DOX引起的心脏毒性的主要靶标。线粒体动力学失衡，以线粒体分裂的增加和线粒体融合的抑制为特征，经常出现在DOX诱导的心脏毒性中，这可能导致过度产生活性氧，能量代谢紊乱，细胞凋亡和其他各种问题。此外，线粒体动力学失调与肿瘤发生也有关。令人惊讶的是，最近的研究表明，靶向线粒体动力学蛋白，如DRP1和MFN2，不仅可以抵御DOX诱导的心脏毒性，还可以增强或不损害其抗癌效果。在本文中，我们总结了DOX诱导的心脏损伤中的线粒体动态失调。此外，我们概述了目前针对参与线粒体动力学的蛋白的药物和非药物干预方法，以减轻DOX引起的心脏损伤。 版权所有©2023 Chen, Niu, Hu和He。

Doxorubicin (DOX) is an extensively used chemotherapeutic agent that can cause severe and frequent cardiotoxicity, which limits its clinical application. Although there have been extensive researches on the cardiotoxicity caused by DOX, there is still a lack of effective treatment. It is necessary to understand the molecular mechanism of DOX-induced cardiotoxicity and search for new therapeutic targets which do not sacrifice their anticancer effects. Mitochondria are considered to be the main target of cardiotoxicity caused by DOX. The imbalance of mitochondrial dynamics characterized by increased mitochondrial fission and inhibited mitochondrial fusion is often reported in DOX-induced cardiotoxicity, which can result in excessive ROS production, energy metabolism disorders, cell apoptosis, and various other problems. Also, mitochondrial dynamics disorder is related to tumorigenesis. Surprisingly, recent studies show that targeting mitochondrial dynamics proteins such as DRP1 and MFN2 can not only defend against DOX-induced cardiotoxicity but also enhance or not impair the anticancer effect. Herein, we summarize mitochondrial dynamics disorder in DOX-induced cardiac injury. Furthermore, we provide an overview of current pharmacological and non-pharmacological interventions targeting proteins involved in mitochondrial dynamics to alleviate cardiac damage caused by DOX.Copyright © 2023 Chen, Niu, Hu and He.