Construction of a mouse model of adriamycin-induced cardiomyopathy

Qingling ZHANG; Yunpeng ZHANG; Zandong ZHOU; Yue ZHANG; Tong LIU

doi:10.19401/j.cnki.1007-3639.2022.10.003

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Construction of a mouse model of adriamycin-induced cardiomyopathy

Specialists'Article | 更新时间：2025-12-31

- Construction of a mouse model of adriamycin-induced cardiomyopathy
- China Oncology Vol. 32, Issue 10, Pages: 948-959(2022)
- 作者机构：
  
  天津医科大学第二医院心脏科，天津市心血管病离子与分子机能重点实验室，天津心脏病学研究所，天津 300211
- 作者简介：
- 基金信息：
- DOI：10.19401/j.cnki.1007-3639.2022.10.003
  CLC： R542.2
- Received：08 August 2022，
  
  Revised：2022-10-18，
  
  Published Online：30 October 2022，
- 稿件说明：
移动端阅览
Qingling ZHANG, Yunpeng ZHANG, Zandong ZHOU, et al. Construction of a mouse model of adriamycin-induced cardiomyopathy[J]. China Oncology, 2022, 32(10): 948-959.
DOI：

Qingling ZHANG, Yunpeng ZHANG, Zandong ZHOU, et al. Construction of a mouse model of adriamycin-induced cardiomyopathy[J]. China Oncology, 2022, 32(10): 948-959. DOI： 10.19401/j.cnki.1007-3639.2022.10.003.

摘要

背景与目的：

阿霉素又称多柔比星，是临床实践中治疗各种肿瘤中有效、应用广泛的细胞毒性化疗药物之一，属于蒽环类抗肿瘤药物。然而该药物会引起严重的不良反应，特别是剂量依赖性心脏毒

性，因而成为肿瘤心脏病学领域颇受关注的问题。目前国际上尚无公认、统一、稳健的阿霉素诱导心肌病模型的构建方法。为探讨最佳给药剂量及频次构建阿霉素诱导急性心肌病设计本实验。

方法：

40只8 ~ 10周龄雄性C57BL/6J小鼠随机分为4组：对照组（control，CON）给予等量生理盐水腹腔注射，以及在阿霉素累积剂量相同的情况下，根据不同给药剂量及频次的M1组（单次给药15 mg/kg）、M2组（单次5 mg/kg，连续3d给药）、M3组（单次7.5 mg/kg，隔天给药，共2次）腹腔注射阿霉素构建阿霉素诱导急性心肌病模型。分别从小鼠一般生命体征、体重变化和存活率、心脏超声、体表心电图、N末端B型利钠肽原（N-terminal pro-B-type natriuretic peptide，NT-proBNP）、心肌肌钙蛋白I（cardiac troponin I，cTnI）及心肌组织形态改变等方面综合评估造模效果。

结果：

与CON相比，M1、M2、M3组小鼠体重均显著下降（

0.001）；M3组较M1和M2组存活率更高（80%

40%、50%，

0.05）。相较于CON、M1组和M2组，体表心电图显示M3组PR间期[（0.064 2±0.003 8）s

（0.042 3±0.000 9）s、（0.052 7±0.007 9）s和（0.062 0±0.001 2）s，

均

0.05

]

、QT间期[（0.047 5±0.000 2）s

（0.022 0±0.000 9）s、（0.038 6±0.004 4）s和（0.044 4±0.003 0）s，

均

0.05

]

显著延长；心脏超声检查结果显示，M3左心室射血分数显著下降（40.40%±2.24%

54.72%±1.64%、46.00%±4.41%和54.68%±3.38%，

均

0.05），M3左心室短轴缩短率显著下降（19.40%±1.20%

27.88%±1.05%、22.57%±2.50%和27.86%±2.20%），差异有统计学意义（

均

0.05）；心脏标志物检测显示，与CON相比，阿霉素给药组M1组、M2组、M3组血清NT-proBNP水平显著升高[（638.13±12.69）pg/mL

（1 271.36±11.76）pg/mL、（1 270.85±36.19）pg/mL和（1 225.26±24.19）pg/mL，

均

0.05）。组织形态学显示，M3心肌细胞空泡化程度及数量显著高于CON、M1和M2（81个/视野

3个/视野、65个/视野、34个/视野，

0.05）。

结论：

腹腔注射阿霉素诱导急性心肌病模型的方法简便、可靠；阿霉素腹腔注射剂量7.5 mg/kg，隔天给药2次，累积剂量15 mg/kg模型最理想。

Abstract

Background and purpose:

Adriamycin also named as doxorubicin

is one of the most widely used cytotoxic chemotherapeutic agents for clinical practice for the treatment of various tumors

and belongs to anthracycline antitumor drugs. Unfortunately

this drug will cause serious side effects

especially dose-dependent cardiotoxicity

which has become a concern in the field of onco-cardiology. At present

there is no universally recognized

unified and ro

bust method to construct Doxorubicin-induced cardiomyopathy model. This experiment was designed to explore the optimal dose and frequency of doxorubicin-induced cardiomyopathy in a mouse model.

Methods:

Forty 8-10-week-old male C57BL/6J mice were randomly divided into 4 groups (control group and 3 model groups). The model group was divided into model 1 (M1) group (15 mg/kg

single dose) and M2 group (5 mg/ kg

once a day for 3 days continuously) and M3 group (7.5 mg/kg

twice on alternate days). General vital signs (body weight change and survival rate)

echocardiography

body surface electrocardiogram (ECG)

N-terminal pro-B-type natriuretic peptide (NT-proBNP)

cardiac troponin I (cTnI) and myocardial tissue morphological changes were evaluated comprehensively.

Results:

Compared with the control group

the body weight of mice in M1

M2 and M3 groups decreased significantly (

0.001); M3 group had higher survival rate than M1 and M2 group (80%

40% and 50%

0.05). Compared with the control group

M1 group and M2 group

the body surface ECG showed that the PR interval of M3 group [(0.064 2±0.003 8)s

(0.042 3±0.000 9)s

(0.052 7±0.007 9) s and (0.062 0±0.001 2)s

0.05

]

and QT interval [(0.047 5±0.000 2)s

(0.022 0±0.000 9)s

(0.038 6±0.004 4)s and (0.044 4±0.003 0)s

0.05

]

were significantly prolonged. Cardiac ultrasound showed that M3 ejection fraction decreased significantly (40.40%±2.24%

54.72%±1.64%

46.00%±4.41% and 54.68%±3.38%

0.05). M3 short-axis shortening rate decreased significantly (19.40%±1.20%

27.88%±1.05%

22.57%±2.50% and 27.86%±2.20%

0.05). Cardiac markers showed that compared with CON

the serum NT-proBNP levels of M1

M2 and M3 in adriamycin group were significantly increased [(638.13±12.69) pg/mL

(1 271.36±11.76) pg/mL

(1 27

0.85±36.19) pg/mL and (1 225.26±24.19) pg/ mL

0.05

]

. Histomorphology showed that the vacuoles in cardiomyocyte of M3 group was significantly increased compared with CON

M1 and M2 group (81/field

3/field

65/field and 34/field

0.05).

Conclusion:

Intraperitoneal injection of adriamycin in acute heart failure model is simple and reliable. The model in which adriamycin is administered by intraperitoneal injection at a dose of 7.5 mg/ kg

twice on alternate days

with cumulative dose of 15 mg/kg is optimal.

关键词

Keywords

references

WILD C P , WEIDERPASS E , STEWART B W , et al. World cancer report: cancer research for cancer prevention . Lyon, France: International Agency for Research on Cancer [R ] , 2020 .

SIEGEL R L , MILLER K D , FUCHS H E , et al. Cancer statistics, 2021 [J ] . CA A Cancer J Clin , 2021 , 71 ( 1 ): 7 - 33 . DOI: 10.3322/caac.21654 http://doi.org/10.3322/caac.21654 https://onlinelibrary.wiley.com/doi/10.3322/caac.21654 https://onlinelibrary.wiley.com/doi/10.3322/caac.21654

ZHENG R S , ZHANG S W , ZENG H M , et al. Cancer incidence and mortality in China, 2016 [J ] . J Natl Cancer Cent , 2022 , 2 ( 1 ): 1 - 9 .

ARMENIAN S H , LACCHETTI C , BARAC A , et al. Prevention and monitoring of cardiac dysfunction in survivors of adult cancers: American Society of Clinical Oncology clinical practice guideline [J ] . J Clin Oncol , 2017 , 35 ( 8 ): 893 - 911 . DOI: 10.1200/JCO.2016.70.5400 http://doi.org/10.1200/JCO.2016.70.5400

ARMENIAN S H , ROBISON L L . Childhood cancer survivorship: an update on evolving paradigms for understanding pathogenesis and screening for therapy-related late effects [J ] . Curr Opin Pediatr , 2013 , 25 ( 1 ): 16 - 22 . DOI: 10.1097/MOP.0b013e32835b0b6a http://doi.org/10.1097/MOP.0b013e32835b0b6a https://journals.lww.com/00008480-201302000-00004 https://journals.lww.com/00008480-201302000-00004

GUDMUNDSDOTTIR T , WINTHER J F , DE FINE LICHT S , et al. Cardiovascular disease in adult life after childhood cancer in Scandinavia: a population-based cohort study of 32 308 one-year survivors [J ] . Int J Cancer , 2015 , 137 ( 5 ): 1176 - 1186 . DOI: 10.1002/ijc.29468 http://doi.org/10.1002/ijc.29468 https://onlinelibrary.wiley.com/doi/10.1002/ijc.29468 https://onlinelibrary.wiley.com/doi/10.1002/ijc.29468

HARVEY V J , SLEVIN M L , PONDER B A , et al. Chemotherapy of diffuse malignant mesothelioma. Phase Ⅱ trials of single-agent 5-fluorouracil and adriamycin [J ] . Cancer , 1984 , 54 ( 6 ): 961 - 964 . DOI: 10.1002/1097-0142(19840915)54:6&lt;961::AID-CNCR2820540602&gt;3.0.CO;2-B http://doi.org/10.1002/1097-0142(19840915)54:6&lt;961::AID-CNCR2820540602&gt;3.0.CO;2-B https://onlinelibrary.wiley.com/doi/10.1002/1097-0142(19840915)54:6&lt;961::AID-CNCR2820540602&gt;3.0.CO;2-B https://onlinelibrary.wiley.com/doi/10.1002/1097-0142(19840915)54:6&lt;961::AID-CNCR2820540602&gt;3.0.CO;2-B

SØRENSEN P G , BACH F , BORK E , et al. Randomized trial of doxorubicin versus cyclophosphamide in diffuse malignant pleural mesothelioma [J ] . Cancer Treat Rep , 1985 , 69 ( 12 ): 1431 - 1432 .

SCHERPEREEL A , BERGHMANS T , LAFITTE J J , et al. Valproate-doxorubicin: promising therapy for progressing mesothelioma. A phase Ⅱ study [J ] . Eur Respir J , 2011 , 37 ( 1 ): 129 - 135 . DOI: 10.1183/09031936.00037310 http://doi.org/10.1183/09031936.00037310 http://erj.ersjournals.com/cgi/doi/10.1183/09031936.00037310 http://erj.ersjournals.com/cgi/doi/10.1183/09031936.00037310

BUIKHUISEN W A , HIDDINGA B I , BAAS P , et al. Second line therapy in malignant pleural mesothelioma: a systematic review [J ] . Lung Cancer , 2015 , 89 ( 3 ): 223 - 231 . DOI: 10.1016/j.lungcan.2015.06.018 http://doi.org/10.1016/j.lungcan.2015.06.018

DIMARCO A , GAETANI M , OREZZI P , et al. “Daunomycin”, a new antibiotic of the rhodomycin group [J ] . Nature , 1964 , 201 : 706 - 707 . DOI: 10.1038/201706a0 http://doi.org/10.1038/201706a0 https://doi.org/10.1038/201706a0 https://doi.org/10.1038/201706a0

CHABNER B A , LONGO D L . Cancer chemotherapy and biotherapy: principles and practice [M ] . Lippincott Williams & Wilkins , 2011 .

COUFAL N , FARNAES L . Anthracyclines and anthraceneodiones[M]//Cancer management in man:chemotherapy, biological therapy , hyperthermia and supporting measures. Dordrecht: Springer Netherlands , 2010 : 87 - 102 .

CURIGLIANO G , CARDINALE D , SUTER T , et al. Cardiovascular toxicity induced by chemotherapy, targeted agents and radiotherapy: ESMO clinical practice guidelines [J ] . Ann Oncol , 2012 , 23 ( Suppl 7 ): Ⅶ155 - 166 .

ZHANG X , HU C , KONG C Y , et al. FNDC5 alleviates oxidative stress and cardiomyocyte apoptosis in doxorubicin-induced cardiotoxicity via activating AKT [J ] . Cell Death Differ , 2020 , 27 ( 2 ): 540 - 555 . DOI: 10.1038/s41418-019-0372-z http://doi.org/10.1038/s41418-019-0372-z

SANGOMLA S , SAIFI M A , KHURANA A , et al. Nanoceria ameliorates doxorubicin induced cardiotoxicity: possible mitigation via reduction of oxidative stress and inflammation [J ] . J Trace Elem Med Biol , 2018 , 47 : 53 - 62 . DOI: S0946-672X(17)30771-X http://doi.org/S0946-672X(17)30771-X

RUSSO M , GUIDA F , PAPARO L , et al. The novel butyrate derivative phenylalanine-butyramide protects from doxorubicin-induced cardiotoxicity [J ] . Eur J Heart Fail , 2019 , 21 ( 4 ): 519 - 528 . DOI: 10.1002/ejhf.1439 http://doi.org/10.1002/ejhf.1439

ZHAO L S , QI Y , XU L N , et al. microRNA-140-5p aggravates doxorubicin-induced cardiotoxicity by promoting myocardial oxidative stress via targeting Nrf2 and Sirt2 [J ] . Redox Biol , 2018 , 15 : 284 - 296 . DOI: S2213-2317(17)30910-2 http://doi.org/S2213-2317(17)30910-2

ZHANG H W , XU A D , SUN X , et al. Self-maintenance of cardiac resident reparative macrophages attenuates doxorubicin-induced cardiomyopathy through the SR-A1-c-Myc axis [J ] . Circ Res , 2020 , 127 ( 5 ): 610 - 627 . DOI: 10.1161/CIRCRESAHA.119.316428 http://doi.org/10.1161/CIRCRESAHA.119.316428

HU C , ZHANG X , WEI W Y , et al. Matrine attenuates oxidative stress and cardiomyocyte apoptosis in doxorubicin-induced cardiotoxicity via maintaining AMPKα/UCP2 pathway [J ] . Acta Pharm Sin B , 2019 , 9 ( 4 ): 690 - 701 . DOI: 10.1016/j.apsb.2019.03.003 http://doi.org/10.1016/j.apsb.2019.03.003 https://linkinghub.elsevier.com/retrieve/pii/S2211383518311511 https://linkinghub.elsevier.com/retrieve/pii/S2211383518311511

TADOKORO T , IKEDA M , IDE T , et al. Mitochondria-dependent ferroptosis plays a pivotal role in doxorubicin cardiotoxicity [J ] . JCI Insight , 2020 , 5 ( 9 ): 132747 .

WANG C Y , CHEN C C , LIN M H , et al. TLR9 binding to beclin 1 and mitochondrial SIRT3 by a sodium-glucose co-transporter 2 inhibitor protects the heart from doxorubicin toxicity [J ] . Biology (Basel) , 2020 , 9 ( 11 ): E369 .

WANG A J , TANG Y F , ZHANG J J , et al. Cardiac SIRT1 ameliorates doxorubicin-induced cardiotoxicity by targeting sestrin 2 [J ] . Redox Biol , 2022 , 52 : 102310 . DOI: 10.1016/j.redox.2022.102310 http://doi.org/10.1016/j.redox.2022.102310 https://linkinghub.elsevier.com/retrieve/pii/S2213231722000829 https://linkinghub.elsevier.com/retrieve/pii/S2213231722000829

FANG X X , WANG H , HAN D , et al. Ferroptosis as a target for protection against cardiomyopathy [J ] . PNAS , 2019 , 116 ( 7 ): 2672 - 2680 . DOI: 10.1073/pnas.1821022116 http://doi.org/10.1073/pnas.1821022116

CHAN B Y H , ROCZKOWSKY A , CHO W J , et al. MMP inhibitors attenuate doxorubicin cardiotoxicity by preventing intracellular and extracellular matrix remodelling [J ] . Cardiovasc Res , 2021 , 117 ( 1 ): 188 - 200 . DOI: 10.1093/cvr/cvaa017 http://doi.org/10.1093/cvr/cvaa017

GUPTA S K , GARG A , BÄR C , et al. Quaking inhibits doxorubicin-mediated cardiotoxicity through regulation of cardiac circular RNA expression [J ] . Circ Res , 2018 , 122 ( 2 ): 246 - 254 . DOI: 10.1161/CIRCRESAHA.117.311335 http://doi.org/10.1161/CIRCRESAHA.117.311335

WU X T , WANG L J , WANG K , et al. ADAR2 increases in exercised heart and protects against myocardial infarction and doxorubicin-induced cardiotoxicity [J ] . Mol Ther , 2022 , 30 ( 1 ): 400 - 414 . DOI: 10.1016/j.ymthe.2021.07.004 http://doi.org/10.1016/j.ymthe.2021.07.004 https://linkinghub.elsevier.com/retrieve/pii/S1525001621003580 https://linkinghub.elsevier.com/retrieve/pii/S1525001621003580

SOKER M , KERVANCIOGLU M . Plasma concentrations of NT-pro-BNP and cardiac troponin-I in relation to doxorubicin-induced cardiomyopathy and cardiac function in childhood malignancy [J ] . Saudi Med J , 2005 , 26 ( 8 ): 1197 - 1202 .

SAWICKI K T , SALA V , PREVER L , et al. Preventing and treating anthracycline cardiotoxicity: new insights [J ] . Annu Rev Pharmacol Toxicol , 2021 , 61 : 309 - 332 . DOI: 10.1146/annurev-pharmtox-030620-104842 http://doi.org/10.1146/annurev-pharmtox-030620-104842

FERRANS V J . Overview of cardiac pathology in relation to anthracycline cardiotoxicity [J ] . Cancer Treat Rep , 1978 , 62 ( 6 ): 955 - 961 .

SHAN K , LINCOFF A M , YOUNG J B . Anthracycline-induced cardiotoxicity [J ] . Ann Intern Med , 1996 , 125 ( 1 ): 47 - 58 .

BERRY G J , JORDEN M . Pathology of radiation and anthracycline cardiotoxicity [J ] . Pediatr Blood Cancer , 2005 , 44 ( 7 ): 630 - 637 .

SWAIN S M , WHALEY F S , EWER M S . Congestive heart failure in patients treated with doxorubicin: a retrospective analysis of three trials [J ] . Cancer , 2003 , 97 ( 11 ): 2869 - 2879 .

JONES L W , HAYKOWSKY M , PEDDLE C J , et al. Cardiovascular risk profile of patients with HER2/neu-positive breast cancer treated with anthracycline-taxane-containing adjuvant chemotherapy and/or trastuzumab [J ] . Cancer Epidemiol Biomarkers Prev , 2007 , 16 ( 5 ): 1026 - 31 . DOI: 10.1158/1055-9965.EPI-06-0870 http://doi.org/10.1158/1055-9965.EPI-06-0870 https://aacrjournals.org/cebp/article/16/5/1026/176788/Cardiovascular-Risk-Profile-of-Patients-with-HER2 https://aacrjournals.org/cebp/article/16/5/1026/176788/Cardiovascular-Risk-Profile-of-Patients-with-HER2

AMIOKA M , SAIRAKU A , OCHI T , et al. Prognostic significance of new-onset atrial fibrillation in patients with non-Hodgkin's lymphoma treated with anthracyclines [J ] . Am J Cardiol , 2016 , 118 ( 9 ): 1386 - 1389 . DOI: S0002-9149(16)31319-4 http://doi.org/S0002-9149(16)31319-4

MAZUR M , WANG F L , HODGE D O , et al. Burden of cardiac arrhythmias in patients with anthracycline-related cardiomyopathy [J ] . JACC Clin Electrophysiol , 2017 , 3 ( 2 ): 139 - 150 . DOI: 10.1016/j.jacep.2016.08.009 http://doi.org/10.1016/j.jacep.2016.08.009 https://linkinghub.elsevier.com/retrieve/pii/S2405500X16302882 https://linkinghub.elsevier.com/retrieve/pii/S2405500X16302882

KILICKAP S , BARISTA I , AKGUL E , et al. Early and late arrhythmogenic effects of doxorubicin [J ] . South Med J , 2007 , 100 ( 3 ): 262 - 265 .

FRADLEY M G , VIGANEGO F , KIP K , et al. Rates and risk of arrhythmias in cancer survivors with chemotherapy-induced cardiomyopathy compared with patients with other cardiomyopathies [J ] . Open Heart , 2017 , 4 ( 2 ): e000701 . DOI: 10.1136/openhrt-2017-000701 http://doi.org/10.1136/openhrt-2017-000701 https://openheart.bmj.com/lookup/doi/10.1136/openhrt-2017-000701 https://openheart.bmj.com/lookup/doi/10.1136/openhrt-2017-000701

QIN Y , GUO T , WANG Z , et al. The role of iron in doxorubicin-induced cardiotoxicity: recent advances and implication for drug delivery [J ] . J Mater Chem B , 2021 , 9 ( 24 ): 4793 - 4803 . DOI: 10.1039/d1tb00551k http://doi.org/10.1039/d1tb00551k

IKEDA S , MATSUSHIMA S , OKABE K , et al. Blockade of L-type Ca2 + channel attenuates doxorubicin-induced cardiomyopathy via suppression of CaMKⅡ-NF-κB pathway [J ] . Sci Rep , 2019 , 9 ( 1 ): 9850 . DOI: 10.1038/s41598-019-46367-6 http://doi.org/10.1038/s41598-019-46367-6 https://doi.org/10.1038/s41598-019-46367-6 https://doi.org/10.1038/s41598-019-46367-6

ZHANG Y S , KNIGHT W , CHEN S , et al. Multiprotein complex with TRPC (transient receptor potential-canonical) channel, PDE1C (phosphodiesterase 1C), and A2R (adenosine A2 receptor) plays a critical role in regulating cardiomyocyte cAMP and survival [J ] . Circulation , 2018 , 138 ( 18 ): 1988 - 2002 . DOI: 10.1161/CIRCULATIONAHA.118.034189 http://doi.org/10.1161/CIRCULATIONAHA.118.034189

HU C , ZHANG X , SONG P , et al. Meteorin-like protein attenuates doxorubicin-induced cardiotoxicity via activating cAMP/PKA/SIRT1 pathway [J ] . Redox Biol , 2020 , 37 : 101747 . DOI: 10.1016/j.redox.2020.101747 http://doi.org/10.1016/j.redox.2020.101747 https://linkinghub.elsevier.com/retrieve/pii/S2213231720309526 https://linkinghub.elsevier.com/retrieve/pii/S2213231720309526

PAN J A , ZHANG H , LIN H , et al. Irisin ameliorates doxorubicin-induced cardiac perivascular fibrosis through inhibiting endothelial-to-mesenchymal transition by regulating ROS accumulation and autophagy disorder in endothelial cells [J ] . Redox Biol , 2021 , 46 : 102120 . DOI: 10.1016/j.redox.2021.102120 http://doi.org/10.1016/j.redox.2021.102120 https://linkinghub.elsevier.com/retrieve/pii/S2213231721002792 https://linkinghub.elsevier.com/retrieve/pii/S2213231721002792

GRATIA S , KAY L , POTENZA L , et al. Inhibition of AMPK signalling by doxorubicin: at the crossroads of the cardiac responses to energetic, oxidative, and genotoxic stress [J ] . Cardiovasc Res , 2012 , 95 ( 3 ): 290 - 299 . DOI: 10.1093/cvr/cvs134 http://doi.org/10.1093/cvr/cvs134

ANJOS M , FONTES-OLIVEIRA M , COSTA V M , et al. An update of the molecular mechanisms underlying doxorubicin plus trastuzumab induced cardiotoxicity [J ] . Life Sci , 2021 , 280 : 119760 . DOI: 10.1016/j.lfs.2021.119760 http://doi.org/10.1016/j.lfs.2021.119760 https://linkinghub.elsevier.com/retrieve/pii/S0024320521007463 https://linkinghub.elsevier.com/retrieve/pii/S0024320521007463

EBRAHIM N , AL SAIHATI H A , MOSTAFA O , et al. Prophylactic evidence of MSCs-derived exosomes in doxorubicin/trastuzumab-induced cardiotoxicity: beyond mechanistic target of NRG-1/erb signaling pathway [J ] . Int J Mol Sci , 2022 , 23 ( 11 ): 5967 . DOI: 10.3390/ijms23115967 http://doi.org/10.3390/ijms23115967 https://www.mdpi.com/1422-0067/23/11/5967 https://www.mdpi.com/1422-0067/23/11/5967

MODESTO P N , POLEGATO B F , DOS SANTOS P P , et al. Green tea (camellia sinensis) extract increased topoisomerase Ⅱ β, improved antioxidant defense, and attenuated cardiac remodeling in an acute doxorubicin toxicity model [J ] . Oxid Med Cell Longev , 2021 , 2021 : 8898919 .

VEJPONGSA P , YEH E . Topoisomerase 2β: a promising molecular target for primary prevention of anthracycline-induced cardiotoxicity [J ] . Clin Pharmacol Ther , 2014 , 95 ( 1 ): 45 - 52 . DOI: 10.1038/clpt.2013.201 http://doi.org/10.1038/clpt.2013.201

BEJI S , D'AGOSTINO M , GAMBINI E , et al. Doxorubicin induces an alarmin-like TLR4-dependent autocrine/paracrine action of nucleophosmin in human cardiac mesenchymal progenitor cells [J ] . BMC Biol , 2021 , 19 ( 1 ): 124 . DOI: 10.1186/s12915-021-01058-5 http://doi.org/10.1186/s12915-021-01058-5

LIU P , BAO H Y , JIN C C , et al. Targeting extracellular heat shock protein 70 ameliorates doxorubicin-induced heart failure through resolution of toll-like receptor 2-mediated myocardial inflammation [J ] . J Am Heart Assoc , 2019 , 8 ( 20 ): e012338 . DOI: 10.1161/JAHA.119.012338 http://doi.org/10.1161/JAHA.119.012338 https://www.ahajournals.org/doi/10.1161/JAHA.119.012338 https://www.ahajournals.org/doi/10.1161/JAHA.119.012338

MA Z G , KONG C Y , WU H M , et al. Toll-like receptor 5 deficiency diminishes doxorubicin-induced acute cardiotoxicity in mice [J ] . Theranostics , 2020 , 10 ( 24 ): 11013 - 11025 . DOI: 10.7150/thno.47516 http://doi.org/10.7150/thno.47516 https://www.thno.org/v10p11013.htm https://www.thno.org/v10p11013.htm

SENEVIRATNE A K , XU M J , HENAO J J A , et al. The mitochondrial transacylase, tafazzin, regulates for AML stemness by modulating intracellular levels of phospholipids [J ] . Cell Stem Cell , 2019 , 24 ( 4 ): 621 - 636 .e16. DOI: S1934-5909(19)30072-4 http://doi.org/S1934-5909(19)30072-4

WANG P X , WANG M H , HU Y H , et al. Isorhapontigenin protects against doxorubicin-induced cardiotoxicity via increasing YAP1 expression [J ] . Acta Pharm Sin B , 2021 , 11 ( 3 ): 680 - 693 . DOI: 10.1016/j.apsb.2020.10.017 http://doi.org/10.1016/j.apsb.2020.10.017 https://linkinghub.elsevier.com/retrieve/pii/S2211383520307693 https://linkinghub.elsevier.com/retrieve/pii/S2211383520307693

XIAO M J , TANG Y F , WANG J (, et al. A new FGF1 variant protects against adriamycin-induced cardiotoxicity via modulating p53 activity [J ] . Redox Biol , 2022 , 49 : 102219 . DOI: 10.1016/j.redox.2021.102219 http://doi.org/10.1016/j.redox.2021.102219 https://linkinghub.elsevier.com/retrieve/pii/S2213231721003797 https://linkinghub.elsevier.com/retrieve/pii/S2213231721003797

SHAIKH F , DUPUIS L L , ALEXANDER S , et al. Cardioprotection and second malignant neoplasms associated with dexrazoxane in children receiving anthracycline chemotherapy: a systematic review and meta-analysis [J ] . J Natl Cancer Inst , 2016 , 108 ( 4 ): djv357 . DOI: 10.1093/jnci/djv357 http://doi.org/10.1093/jnci/djv357 https://academic.oup.com/jnci/article-lookup/doi/10.1093/jnci/djv357 https://academic.oup.com/jnci/article-lookup/doi/10.1093/jnci/djv357

JIRKOVSKÁ A , KARABANOVICH G , KUBEŠ J , et al. Structure-activity relationship study of dexrazoxane analogues reveals ICRF-193 as the most potent bisdioxopiperazine against anthracycline toxicity to cardiomyocytes due to its strong topoisomerase Ⅱβ interactions [J ] . J Med Chem , 2021 , 64 ( 7 ): 3997 - 4019 . DOI: 10.1021/acs.jmedchem.0c02157 http://doi.org/10.1021/acs.jmedchem.0c02157 https://pubs.acs.org/doi/10.1021/acs.jmedchem.0c02157 https://pubs.acs.org/doi/10.1021/acs.jmedchem.0c02157

TEBBI C K , LONDON W B , FRIEDMAN D , et al. Dexrazoxane-associated risk for acute myeloid leukemia/myelodysplastic syndrome and other secondary malignancies in pediatric Hodgkin's disease [J ] . J Clin Oncol , 2007 , 25 ( 5 ): 493 - 500 .

HORACEK J M , JAKL M , HORACKOVA J , et al. Assessment of anthracycline-induced cardiotoxicity with electrocardiography [J ] . Exp Oncol , 2009 , 31 ( 2 ): 115 - 117 .

ARBEL Y , SWARTZON M , JUSTO D . QT prolongation and Torsades de Pointes in patients previously treated with anthracyclines [J ] . Anticancer Drugs , 2007 , 18 ( 4 ): 493 - 498 . DOI: 10.1097/CAD.0b013e328012d023 http://doi.org/10.1097/CAD.0b013e328012d023 https://journals.lww.com/00001813-200704000-00016 https://journals.lww.com/00001813-200704000-00016

TAKEMURA G , FUJIWARA H . Doxorubicin-induced cardiomyopathy from the cardiotoxic mechanisms to management [J ] . Prog Cardiovasc Dis , 2007 , 49 ( 5 ): 330 - 352 .

KUNO A , HOSODA R , TSUKAMOTO M , et al. SIRT1 in the cardiomyocyte counteracts doxorubicin-induced cardiotoxicity via regulating histone H2AX [J ] . Cardiovasc Res , 2022 : cvac026 .

SINGAL P K , ILISKOVIC N . Doxorubicin-induced cardiomyopathy [J ] . N Engl J Med , 1998 , 339 ( 13 ): 900 - 5 . DOI: 10.1056/NEJM199809243391307 http://doi.org/10.1056/NEJM199809243391307 http://www.nejm.org/doi/abs/10.1056/NEJM199809243391307 http://www.nejm.org/doi/abs/10.1056/NEJM199809243391307

SHEN Y H , ZHANG H , NI Y Y , et al. Tripartite motif 25 ameliorates doxorubicin-induced cardiotoxicity by degrading p85α [J ] . Cell Death Dis , 2022 , 13 ( 7 ): 643 . DOI: 10.1038/s41419-022-05100-4 http://doi.org/10.1038/s41419-022-05100-4

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