Mitochondria-Targeting Small Molecules Effectively Prevent Cardiotoxicity Induced by Doxorubicin.

Mitochondria-Targeting Small Molecules Effectively Prevent Cardiotoxicity Induced by Doxorubicin.
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靶向线粒体的小分子有效预防阿霉素引起的心脏毒性

DOI:
10.3390/molecules23061486
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发表时间:
2018-06-19
期刊:
Molecules (Basel, Switzerland)
影响因子:
--
通讯作者:
Cui G
Cui G
中科院分区:
其他
文献类型:
--
作者:
Shi W;Deng H;Zhang J;Zhang Y;Zhang X;Cui G

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多柔比星(Dox)是广泛用于治疗多种癌症的化学治疗剂。然而,Dox的临床使用受到其不必要的心脏毒性的限制。线粒体功能障碍与Dox诱导的心脏毒性有关。为了减轻Dox相关的心脏毒性,近年来出现了大量靶向线粒体的小分子调节Dox诱导的心脏毒性的成功例子。本文综述了近年来的相关文献,并对靶向靶向小分子药物作为抗Dox心脏事件的心脏保护剂的研究进展进行了讨论。
Doxorubicin (Dox) is a chemotherapeutic agent widely used for the treatment of numerous cancers. However, the clinical use of Dox is limited by its unwanted cardiotoxicity. Mitochondrial dysfunction has been associated with Dox-induced cardiotoxicity. To mitigate Dox-related cardiotoxicity, considerable successful examples of a variety of small molecules that target mitochondria to modulate Dox-induced cardiotoxicity have appeared in recent years. Here, we review the related literatures and discuss the evidence showing that mitochondria-targeting small molecules are promising cardioprotective agents against Dox-induced cardiac events.
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