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1
Mice lacking mitochondrial ferritin are more sensitive to doxorubicin-mediated cardiotoxicity.缺乏线粒体铁蛋白的小鼠对阿霉素介导的心脏毒性更敏感。
J Mol Med (Berl). 2014 Aug;92(8):859-69. doi: 10.1007/s00109-014-1147-0. Epub 2014 Apr 13.
2
Mitochondrial topoisomerase I (top1mt) is a novel limiting factor of doxorubicin cardiotoxicity.线粒体拓扑异构酶I（top1mt）是阿霉素心脏毒性的一种新型限制因素。
Clin Cancer Res. 2014 Sep 15;20(18):4873-81. doi: 10.1158/1078-0432.CCR-13-3373. Epub 2014 Apr 8.
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The role of iron in anthracycline cardiotoxicity.铁在蒽环类药物心脏毒性中的作用。
Front Pharmacol. 2014 Feb 26;5:25. doi: 10.3389/fphar.2014.00025. eCollection 2014.
4
Topoisomerase 2β: a promising molecular target for primary prevention of anthracycline-induced cardiotoxicity.拓扑异构酶 2β：蒽环类抗生素诱导心脏毒性一级预防的有前途的分子靶标。
Clin Pharmacol Ther. 2014 Jan;95(1):45-52. doi: 10.1038/clpt.2013.201. Epub 2013 Oct 3.
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Negative regulation of mitochondrial transcription by mitochondrial topoisomerase I.线粒体拓扑异构酶 I 对线粒体转录的负调控。
Nucleic Acids Res. 2013 Nov;41(21):9848-57. doi: 10.1093/nar/gkt768. Epub 2013 Aug 27.
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Identification of the molecular basis of doxorubicin-induced cardiotoxicity.鉴定多柔比星致心肌病的分子基础。
Nat Med. 2012 Nov;18(11):1639-42. doi: 10.1038/nm.2919. Epub 2012 Oct 28.
7
Mitochondrial topoisomerase I is critical for mitochondrial integrity and cellular energy metabolism.线粒体拓扑异构酶 I 对于线粒体的完整性和细胞能量代谢至关重要。
PLoS One. 2012;7(7):e41094. doi: 10.1371/journal.pone.0041094. Epub 2012 Jul 20.
8
Oxidative stress, redox signaling, and metal chelation in anthracycline cardiotoxicity and pharmacological cardioprotection.蒽环类药物心脏毒性的氧化应激、氧化还原信号和金属螯合作用及药理学心脏保护作用。
Antioxid Redox Signal. 2013 Mar 10;18(8):899-929. doi: 10.1089/ars.2012.4795. Epub 2012 Oct 12.
9
Dexrazoxane for the prevention of cardiac toxicity and treatment of extravasation injury from the anthracycline antibiotics.地塞米松预防蒽环类抗生素心脏毒性和外渗损伤的治疗。
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10
Targeting DNA topoisomerase II in cancer chemotherapy.癌症化疗中靶向DNA拓扑异构酶II
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扭转与熨烫：线粒体DNA损伤导致的阿霉素心脏毒性

Twisting and ironing: doxorubicin cardiotoxicity by mitochondrial DNA damage.

作者信息

Nitiss Karin C, Nitiss John L

机构信息

Biomedical Sciences Department, UIC College of Medicine and Department of Biopharmaceutical Sciences, UIC College of Pharmacy, Rockford, Illinois.

出版信息

Clin Cancer Res. 2014 Sep 15;20(18):4737-9. doi: 10.1158/1078-0432.CCR-14-0821. Epub 2014 Jun 10.

DOI:10.1158/1078-0432.CCR-14-0821
PMID:24916696
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4204112/
Abstract

Anthracyclines are active clinical agents that have multiple mechanisms of cytotoxicity. Cardiotoxicity by anthracyclines limits the therapeutic potential of these agents, but mechanisms leading to cardiotoxicity remain controversial. Transgenic mice that lack mitochondrial topoisomerase I are hypersensitive to doxorubicin cardiotoxicity, providing support for cardiotoxicity arising from damage of mitochondrial DNA.

摘要

蒽环类药物是具有多种细胞毒性机制的活性临床药物。蒽环类药物引起的心脏毒性限制了这些药物的治疗潜力，但导致心脏毒性的机制仍存在争议。缺乏线粒体拓扑异构酶I的转基因小鼠对阿霉素心脏毒性高度敏感，这为线粒体DNA损伤引起的心脏毒性提供了支持。