Identification of the molecular basis of doxorubicin-induced cardiotoxicity

Doxorubicin, which induces tumor cell death through effects on topoisomerase-II, is a commonly used chemotherapeutic agent but has the substantial drawback of causing cardiotoxicity. Edward T.H.Yeh and his colleagues now show that doxorubicin-induced cardiotoxicity in mice is due to the deleterious...

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Published in	Nature medicine Vol. 18; no. 11; pp. 1639 - 1642
Main Authors	Zhang, Sui, Liu, Xiaobing, Bawa-Khalfe, Tasneem, Lu, Long-Sheng, Lyu, Yi Lisa, Liu, Leroy F, Yeh, Edward T H
Format	Journal Article
Language	English
Published	New York Nature Publishing Group US 01.11.2012 Nature Publishing Group
Subjects	631/92/609 692/699/75 692/700/565/2194 Animals Apoptosis - drug effects Biomedicine brief-communication Cancer Research Cardiology Cardiotoxins Complications and side effects Deoxyribonucleic acid DNA DNA Topoisomerases, Type II - genetics DNA-Binding Proteins - genetics Doxorubicin Doxorubicin - toxicity Heart Failure - chemically induced Humans Infectious Diseases Metabolic Diseases Mice Mitochondrial Turnover - drug effects Molecular biology Molecular Medicine Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Neurosciences Physiological aspects Poly-ADP-Ribose Binding Proteins Reactive Oxygen Species - metabolism Sequence Deletion Toxicity
Online Access	Get full text
ISSN	1078-8956 1546-170X 1546-170X
DOI	10.1038/nm.2919

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Abstract	Doxorubicin, which induces tumor cell death through effects on topoisomerase-II, is a commonly used chemotherapeutic agent but has the substantial drawback of causing cardiotoxicity. Edward T.H.Yeh and his colleagues now show that doxorubicin-induced cardiotoxicity in mice is due to the deleterious effects of doxorubicin on topoisomerase-IIβ in cardiomyocytes, leading to alterations in gene expression, mitochondrial dysfunction and cell death. Doxorubicin is believed to cause dose-dependent cardiotoxicity through redox cycling and the generation of reactive oxygen species (ROS). Here we show that cardiomyocyte-specific deletion of Top2b (encoding topoisomerase-IIβ) protects cardiomyocytes from doxorubicin-induced DNA double-strand breaks and transcriptome changes that are responsible for defective mitochondrial biogenesis and ROS formation. Furthermore, cardiomyocyte-specific deletion of Top2b protects mice from the development of doxorubicin-induced progressive heart failure, suggesting that doxorubicin-induced cardiotoxicity is mediated by topoisomerase-IIβ in cardiomyocytes.
AbstractList	Doxorubicin, which induces tumor cell death through effects on topoisomerase-II, is a commonly used chemotherapeutic agent but has the substantial drawback of causing cardiotoxicity. Edward T.H.Yeh and his colleagues now show that doxorubicin-induced cardiotoxicity in mice is due to the deleterious effects of doxorubicin on topoisomerase-IIβ in cardiomyocytes, leading to alterations in gene expression, mitochondrial dysfunction and cell death. Doxorubicin is believed to cause dose-dependent cardiotoxicity through redox cycling and the generation of reactive oxygen species (ROS). Here we show that cardiomyocyte-specific deletion of Top2b (encoding topoisomerase-IIβ) protects cardiomyocytes from doxorubicin-induced DNA double-strand breaks and transcriptome changes that are responsible for defective mitochondrial biogenesis and ROS formation. Furthermore, cardiomyocyte-specific deletion of Top2b protects mice from the development of doxorubicin-induced progressive heart failure, suggesting that doxorubicin-induced cardiotoxicity is mediated by topoisomerase-IIβ in cardiomyocytes. Doxorubicin is believed to cause dose-dependent cardiotoxicity through redox cycling and the generation of reactive oxygen species (ROS). Here we show that cardiomyocyte-specific deletion of Top2b (encoding topoisomerase-IIβ) protects cardiomyocytes from doxorubicin-induced DNA double-strand breaks and transcriptome changes that are responsible for defective mitochondrial biogenesis and ROS formation. Furthermore, cardiomyocyte-specific deletion of Top2b protects mice from the development of doxorubicin-induced progressive heart failure, suggesting that doxorubicin-induced cardiotoxicity is mediated by topoisomerase-IIβ in cardiomyocytes. Doxorubicin is believed to cause dose-dependent cardiotoxicity through redox cycling and the generation of reactive oxygen species (ROS). Here we show that cardiomyocyte-specific deletion of Top2b (encoding topoisomerase-IIβ) protects cardiomyocytes from doxorubicin-induced DNA double-strand breaks and transcriptome changes that are responsible for defective mitochondrial biogenesis and ROS formation. Furthermore, cardiomyocyte-specific deletion of Top2b protects mice from the development of doxorubicin-induced progressive heart failure, suggesting that doxorubicin-induced cardiotoxicity is mediated by topoisomerase-IIβ in cardiomyocytes.Doxorubicin is believed to cause dose-dependent cardiotoxicity through redox cycling and the generation of reactive oxygen species (ROS). Here we show that cardiomyocyte-specific deletion of Top2b (encoding topoisomerase-IIβ) protects cardiomyocytes from doxorubicin-induced DNA double-strand breaks and transcriptome changes that are responsible for defective mitochondrial biogenesis and ROS formation. Furthermore, cardiomyocyte-specific deletion of Top2b protects mice from the development of doxorubicin-induced progressive heart failure, suggesting that doxorubicin-induced cardiotoxicity is mediated by topoisomerase-IIβ in cardiomyocytes.
Audience	Academic
Author	Liu, Xiaobing Lyu, Yi Lisa Lu, Long-Sheng Zhang, Sui Bawa-Khalfe, Tasneem Liu, Leroy F Yeh, Edward T H
Author_xml	– sequence: 1 givenname: Sui surname: Zhang fullname: Zhang, Sui organization: Department of Cardiology, The University of Texas MD Anderson Cancer Center – sequence: 2 givenname: Xiaobing surname: Liu fullname: Liu, Xiaobing organization: Texas Heart Institute at St. Luke's Episcopal Hospital, Department of Vascular Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine – sequence: 3 givenname: Tasneem surname: Bawa-Khalfe fullname: Bawa-Khalfe, Tasneem organization: Department of Cardiology, The University of Texas MD Anderson Cancer Center – sequence: 4 givenname: Long-Sheng surname: Lu fullname: Lu, Long-Sheng organization: Texas Heart Institute at St. Luke's Episcopal Hospital – sequence: 5 givenname: Yi Lisa surname: Lyu fullname: Lyu, Yi Lisa organization: Department of Pharmacology, University of Medicine and Dentistry of New Jersey—Robert Wood Johnson Medical School – sequence: 6 givenname: Leroy F surname: Liu fullname: Liu, Leroy F organization: Department of Pharmacology, University of Medicine and Dentistry of New Jersey—Robert Wood Johnson Medical School – sequence: 7 givenname: Edward T H surname: Yeh fullname: Yeh, Edward T H email: etyeh@mdanderson.org organization: Department of Cardiology, The University of Texas MD Anderson Cancer Center, Texas Heart Institute at St. Luke's Episcopal Hospital
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/23104132$$D View this record in MEDLINE/PubMed
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Snippet	Doxorubicin, which induces tumor cell death through effects on topoisomerase-II, is a commonly used chemotherapeutic agent but has the substantial drawback of... Doxorubicin is believed to cause dose-dependent cardiotoxicity through redox cycling and the generation of reactive oxygen species (ROS). Here we show that...
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SubjectTerms	631/92/609 692/699/75 692/700/565/2194 Animals Apoptosis - drug effects Biomedicine brief-communication Cancer Research Cardiology Cardiotoxins Complications and side effects Deoxyribonucleic acid DNA DNA Topoisomerases, Type II - genetics DNA-Binding Proteins - genetics Doxorubicin Doxorubicin - toxicity Heart Failure - chemically induced Humans Infectious Diseases Metabolic Diseases Mice Mitochondrial Turnover - drug effects Molecular biology Molecular Medicine Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Neurosciences Physiological aspects Poly-ADP-Ribose Binding Proteins Reactive Oxygen Species - metabolism Sequence Deletion Toxicity
Title	Identification of the molecular basis of doxorubicin-induced cardiotoxicity
URI	https://link.springer.com/article/10.1038/nm.2919 https://www.ncbi.nlm.nih.gov/pubmed/23104132 https://www.proquest.com/docview/1144924496 https://www.proquest.com/docview/1151032323
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