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Screening of Myocardial cardiotoxicity Induced by Anticancer Chemotherapy and the Importance of Global Longitudinal Strain

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World Journal of Cardiovascular Diseases 2024年第6期14卷 381-391页

作者： Marguerite Téning Diouf Fatou Aw Hussein Khadra Sophie Ba Doudou Diouf Michel Ngonar Sarr Joseph Salvador Mingou Malick Ndiaye Simon Antoine Sarr Momar Dioum Aliou Alassane Ngaide Serigne Mor Beye Simon Manga Alain Affangla Youssou Diouf Khadimu Rassoul Diop Malick Bodian Mohamed Leye Mouhamadou Bamba Ndiaye Alassane Mbaye Adama Kane Maboury Diao Abdoul Kane Cardiology Department of the Dalal Jamm Hospital Dakar Senegal Cardiology Department Hospital Aristide Le Dantec Dakar Senegal Cardiology Department Hospital Fann Dakar Senegal UFR2S Saint Louis Saint Louis Senegal UFR Ziguinchor Ziguinchor Senegal Training and Research in Health Sciences Unit University of Thies Thies Senegal Cardiology Department Hospital General Idrissa Pouye Dakar Senegal

Introduction: The improvement of survival in patients with cancer and the expansion of therapeutic options have led to the emergence of a new profile of cardiotoxicity, specifically associated with antimitotic agents. Our study aimed to assess the incidence of chemotherapy-induced myocardial toxicity in patients with cancer. Patients and Methods: We conducted a looking-forward longitudinal cohort study including all patients admitted to the Cardiology departments of Aristide le Dantec Hospital and Dalal Jamm National Hospital Centre for apre-chemotherapy check-up. The included patients did not undergo any pre-existing cardiopathy. Results: Over a period of two years ranging from January 2019 to December 2021, a total of 37 patients were included in the study. Notably, there was a female predominance (92%) with an average age of 49.7 years ± 13.69. Breast cancer accounted for 70% of the neoplasms. Laboratory findings revealed moderate anemia in 19 patients (51%). At inclusion, the left ventricle (LV) was of normal size (LV diastole at 44.46 ± 4.97 mm). The systolic function of the left ventricle was normal in all patients, with an average ejection fraction (EF) of 63.1% ± 5.80 and a mean global longitudinal strain (GLS) of −20.4% ± 2.58. The most commonly used agents were anthracyclines. During follow-up, 3 patients (8.1%) developed clinical symptoms of left heart failure, and LV dysfunction on echocardiography was observed in 5 (13.5%) patients, with a significant decrease in EF Conclusion: The incidence of cardiac toxicity is not negligible, hence the importance of early screening. Strain imaging is an essential tool that should be performed as part of the assessment before chemotherapy and re-evaluated during treatment.

关键词： Cancer Chemotherapy Global Longitudinal Strain cardiotoxicity

Mepanipyrim induces cardiotoxicity of zebrafish(Danio rerio) larvae via promoting AhR-regulated COX expression pathway

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Journal of Environmental Sciences 2023年第3期125卷 650-661页

作者： Chao Shen Jing He Kongyang Zhu Naying Zheng Yue Yu Chengyong He Chunyan Yang Zhenghong Zuo State Key Laboratory of Cellular Stress Biology School of Life SciencesXiamen UniversityXiamen 361005China State Key Laboratory of Marine Environmental Science Xiamen UniversityXiamen 361005China

The wide use of pesticides has seriously threatened human health and the survival of beneficial organisms. The fungicide mepanipyrim is widely used in viticulture practices. Studies of mepanipyrim-induced toxicity in organisms are still scarce, especially studies on cardiotoxicity. In this study, we aimed to investigate mepanipyrim-induced cardiotoxicity in zebrafish(Danio rerio) larvae. We found that mepanipyrim could induce cardiotoxicity by altering the heart rate and cardiomyocyte diameter of larvae. Meanwhile, RNA sequencing and RT-qPCR data indicated that mepanipyrim exposure could dramatically alter the m RNA expression of calcium signaling pathway-, cardiac muscle contraction-, and oxidative respiratory chain-related genes. Interestingly, by the CALUX cell bioassay, we found that most cytochrome c oxidase(COX) family genes exhibited potential AhR-regulated activity, suggesting that mepanipyrim induced cardiotoxicity via a novel AhR-regulated manner in ***, the AhR antagonist CH_(2)23191 could effectively prevent mepanipyrim-induced cardiotoxicity in zebrafish larvae. In conclusion, the AhR agonist mepanipyrim could induce cardiotoxicity in a novel unreported AhR-regulated manner, which could specifically affect the expression of COX family genes involved in the mitochondrial oxidative respiratory chain. Our data will help explain the toxic effects of mepanipyrim on organisms and provide new insight into the AhR agonistic activity pesticide-induced cardiotoxicity.

关键词： Zebrafish(Danio rerio) Mepanipyrim AhR agonist cardiotoxicity CH_(2)23191 Cytochrome coxidase

cardiotoxicity of current antipsychotics:Newer antipsychotics or adjunct therapy?

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World Journal of Psychiatry 2022年第8期12卷 1108-1111页

作者： Zheng Liu Mo-Lin Zhang Xin-Ru Tang Xiao-Qing Li Jing Wang Li-Liang Li Department of Forensic Medicine School of Basic Medical SciencesFudan UniversityShanghai 200032China

Use of newer antipsychotics for substitution of current antipsychotics might be one way awaiting to be clinically verified to address antipsychotic cardiotoxic ***,the combination of existing antipsychotics with cardioprotective agents is also beneficial for patients with mental disorders for avoiding cardiotoxicity to the maximum.

关键词： Antipsychotics cardiotoxicity Combined medication Adjunct therapy

TBC1D15 deficiency protects against doxorubicin cardiotoxicity via inhibiting DNAPKcs cytosolic retention and DNA damage

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Acta Pharmaceutica Sinica B 2023年第12期13卷 4823-4839页

作者： Wenjun Yu Haixia Xu Zhe Sun Yuxin Du Shiqun Sun Miyesaier Abudureyimu Mengjiao Zhang Jun Tao Junbo Ge Jun Ren Yingmei Zhang Department of Cardiology and Shanghai Institute of Cardiovascular Diseases Zhongshan HospitalFudan UniversityShanghai 200032China National Clinical Research Center for Interventional Medicine Shanghai 200032China Department of Cardiovascular Surgery Zhongnan Hospital of Wuhan UniversityWuhan 430071China Hubei Provincial Engineering Research Center of Minimally Invasive Cardiovascular Surgery Wuhan 430071China Department of Cardiology Affiliated Hospital of Nantong UniversityNantong 226001China Cardiovascular Department Shanghai Xuhui Central HospitalZhongshan-Xuhui HospitalFudan UniversityShanghai 200030China Department of Cardiovascular Surgery Sun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhou 510000China

Clinical application of doxorubicin(DOX)is heavily hindered by DOX *** theories were postulated for DOX cardiotoxicity including DNA damage and DNA damage response(DDR),although the mechanism(s)involved remains to be *** study evaluated the potential role of TBC domain family member 15(TBC1D15)in DOX ***-induced cardiac-specific Tbcldi5 knockout(Tbcldi5^(CKO))or Tbcldi5 knockin(Tbcldi5^(CKI))male mice were challenged with a single dose of DOx prior to cardiac assessment 1 week or 4 weeks following DOX *** encoding TBC1D15 or containing shRNA targeting Tbcld15 were used for Tbcld15 overexpression or knockdown in isolated primary mouse *** results re-vealed that DOX evoked upregulation of TBC1D15 with compromised myocardial function and overt mortality,the effects of which were ameliorated and accentuated by Tbcldi5 deletion and Tbcld15 overexpression,*** overtly evoked apoptotic cell death,the effect of which was alleviated and exacerbated by Tbcld15 knockout and overexpression,***,DOX provoked mitochondrial membrane potential collapse,oxidative stress and DNA damage,the effects of which were mitigated and exacerbated by Tbcld15 knockdown and overexpression,*** scrutiny revealed that TBC1D15 fostered cytosolic accumulation of the cardinal DDR element DNA-dependent protein kinase catalytic subunit(DNA-PKcs).Liquid chromatography-tandem mass spectrometry and coimmunoprecipitation denoted an interaction between TBCID15 and DNA-PKcs at the segment 594-624 of ***,overexpression of TBC1D15 mutant(A594-624,deletion of segment 594-624)failed to elicit accentuation of DOX-induced cytosolic retention of DNA-PKcs,DNA damage and cardiomyocyte apoptosis by TBC1D15 wild ***,Tbcld15 deletion ameliorated DOXinduced cardiomyocyte contractile anomalies,apoptosis,mitochondrial anomalies,DNA damage and cytosolic DNA-PKcs accumulatio

关键词： Doxorubicin cardiotoxicity DNA damage DNA damage response Mitochondrial anomalies Cardiomyocyte apoptosis TBC1D15 DNA-PKcS

Shengmai San for Treatment of cardiotoxicity from Anthracyclines:A Systematic Review and Meta-Analysis

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Chinese Journal of Integrative Medicine 2022年第4期28卷 374-383页

作者： ZHANG Xiao-nan LI Yan-yang ZHANG Yuan-hui ZHANG Wan-qin ZHU Ya-ping ZHANG Jun-ping LV Shi-chao LIU Long-tao National Clinical Research Center for Chinese Medicine Cardiology Xiyuan HospitalChina Academy of Chinese Medical SciencesBeijing100091China Tianjin Medical University Cancer Institute and Hospital Tianjin300060China First Teaching Hospital of Tianjin University of Traditional Chinese Medicine Tianjin300112China

Objective:To systematically evaluate the efficacy of Shengmai San in patients with cardiotoxicity of ***:Randomized controlled trials(RCTs)were identified by searching China National Knowledge Infrastructure(CNKI),Wanfang Database,Chinese Biomedical Literature Database(CBM),Pub Med,Cochrane Library,and Embase Databases from the inceptions until December *** Cochrane Handbook was used to evaluate the risk of bias in the included *** analysis was conducted using Rev Man 5.3 ***:Totally 19 RCTs with 2,331 participants were included in this *** showed that in improving arrhythmia(13 RCTs,n=1,877,RR=0.37,95%CI 0.25 to 0.52,Pcardiotoxicity from ***,in the future,it is still necessary to conduct high-quality RCTs to verify its efficacy.

关键词： Shengmai San anthracyclines cardiotoxicity systematic review meta-analysis

Overexpressed SIRT6 ameliorates doxorubicin-induced cardiotoxicity and potentiates the therapeutic efficacy through metabolic remodeling

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药学学报:英文版 2023年第6期13卷 2680-2700页

作者： Kezheng Peng Chenye Zeng Yuqi Gao Binliang Liu Liyuan Li Kang Xu Yuemiao Yin Ying Qiu Mingkui Zhang Fei Ma Zhao Wang The Ministry of Education Key Laboratory of Protein Science School of Pharmaceutical SciencesTsinghua UniversityBeijing 100084China Department of Medical Oncology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China School of Medicine Tsinghua UniversityBeijing 100084China Department of Cardiac Surgery First Hospital of Tsinghua UniversityBeijing 100016China

Since the utilization of anthracyclines in cancer therapy, severe cardiotoxicity has become a major obstacle. The major challenge in treating cancer patients with anthracyclines is minimizing cardiotoxicity without compromising antitumor efficacy. Herein, histone deacetylase SIRT6 expression was reduced in plasma of patients treated with anthracyclines-based chemotherapy regimens. Furthermore,overexpression of SIRT6 alleviated doxorubicin-induced cytotoxicity in cardiomyocytes, and potentiated cytotoxicity of doxorubicin in multiple cancer cell lines. Moreover, SIRT6 overexpression ameliorated doxorubicin-induced cardiotoxicity and potentiated antitumor efficacy of doxorubicin in mice, suggesting that SIRT6 overexpression could be an adjunctive therapeutic strategy during doxorubicin ***, doxorubicin-impaired mitochondria led to decreased mitochondrial respiration and ATP production. And SIRT6 enhanced mitochondrial biogenesis and mitophagy by deacetylating and inhibiting Sgk1. Thus, SIRT6 overexpression coordinated metabolic remodeling from glycolysis to mitochondrial respiration during doxorubicin treatment, which was more conducive to cardiomyocyte metabolism, thus protecting cardiomyocytes but not cancer cells against doxorubicin-induced energy deficiency. In addition, ellagic acid, a natural compound that activates SIRT6, alleviated doxorubicininduced cardiotoxicity and enhanced doxorubicin-mediated tumor regression in tumor-bearing *** findings provide a preclinical rationale for preventing cardiotoxicity by activating SIRT6 in cancer patients undergoing chemotherapy, but also advancing the understanding of the crucial role of SIRT6 in mitochondrial homeostasis.

关键词： SIRT6 Doxorubicin cardiotoxicity Antitumor efficacy Ellagic acid Mitochondrial homeostasis Glycolysis SGK1

Phloretin-induced suppression of oxidative and nitrosative stress attenuates doxorubicin-induced cardiotoxicity in rats

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Asian Pacific Journal of Tropical Biomedicine 2022年第3期12卷 124-131页

作者： Shivani S.Wagh Kalpesh R.Patil Umesh B.Mahajan Pradnya D.Bagal Avinash R.Wadkar Basavraj Bommanhalli Prabhakar R.Patil Sameer N.Goyal Shreesh Ojha Chandragouda R.Patil Department of Pharmacology R.C.Patel Institute of Pharmaceutical Education and ResearchShirpur-425405Dist.DhuleMaharashtraIndia Department of Pathology Gadag Institute of Medical SciencesGadagKarnatakaIndia Department of Pharmacology Navodaya Medical CollegePost Box No:26Mantralayam RoadNavodaya NagarRaichur-584103KarnatakaIndia Shri Vile Parle Kelavani Mandal's Institute of Pharmacy Dhule-424001MaharashtraIndia Department of Pharmacology and Therapeutics College of Medicine and Health SciencesUnited Arab Emirates UniversityP.O.Box 17666Al AinAbu DhabiUAE Department of Pharmacology Delhi Pharmaceutical Sciences and Research UniversityMehrauli-Badarpur RoadPushp Vihar Sector-3New Delhi-110017India

Objective:To compare the cardioprotective efficacy of equimolar doses(50 mM/kg,p.o.)of phloretin and genistein against doxorubicin-induced cardiotoxicity in ***:cardiotoxicity was induced in rats by intraperitoneal injection of 6 mg/kg doxorubicin on alternative days till the cumulative dose reached 30 mg/*** study included four treatment groups of rats(n=6):the control group(0.5%carboxymethyl cellulose solution-treated),the doxorubicin-treated group(0.5%carboxymethyl cellulose solution along with doxorubicin),the genistein-treated group(50 mM/kg/day;*** with doxorubicin)and phloretin-treated group(50 mM/kg/day;*** with doxorubicin).On the 10th day of dosing,rats were anesthetized for recording ECG,mean arterial pressure,and left ventricular *** stress,nitric oxide levels,and inflammatory cytokines were estimated in the cardiac *** function parameters(creatine kinase MB,lactate dehydrogenase,aspartate aminotransferase,and alanine transaminase)were estimated in the serum ***:Phloretin treatment inhibited doxorubicin-induced oxidative stress and also reduced nitric oxide levels in cardiac tissues of *** administration attenuated doxorubicin-induced alterations in hemodynamic parameters(heart rate,mean arterial blood pressure,and left ventricular function)and suppressed the expression of pro-inflammatory *** cardiac injury markers like creatine kinase MB,lactate dehydrogenase,aspartate aminotransferase,and alanine transaminase were reduced by both genistein and *** these effects of phloretin were more prominent than ***:Phloretin offers cardioprotection that is comparable to genistein,a clinically validated cardioprotectant against doxorubicin-induced *** studies are needed to confirm and establish the therapeutic utility of phloretin as a chemopreventive adjuvant to doxorubicin chemotherapy.

关键词： cardiotoxicity Chemoprevention Doxorubicin Genistein Phloretin Phytoestrogens Cardiac injury Hemodynamic changes

Didymin attenuates doxorubicin-induced cardiotoxicity by inhibiting oxidative stress

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Chinese Herbal Medicines 2022年第1期14卷 70-78页

作者： Rongchang Chen Guibo Sun Lijiao Xu Xu Zhang Wenying Zeng Xiaobo Sun Institute of Medicinal Plant Development Peking Union Medical College and Chinese Academy of Medical SciencesBeijing 100193China Department of Comprehensive Medicine Xiyuan HospitalChina Academy of Chinese Medical SciencesBeijing 100091China

Objective:This study was designed to investigate the protective effects of didymin(Did)on doxorubicin(DOX)-induced ***:After pretreatment with Did(2,4,8 mg/kg intraperitoneal i.p.)for 7 d,the male C57 mice were injected with single dose of DOX(20 mg/kg i.p.).The cardioprotective effect of Did was observed on the 7th day after DOX ***:DOX delayed body growth and caused cardiac tissue injury,oxidative stress,and mitochondrial *** experiments in H9C2 cardiomyocytes showed that DOX reduced cell viability,increased generation of reactive oxygen species(ROS)and fragmentation of DNA,decreased mitochondrial membrane potential,and induced cardiomyocyte ***,all of these adverse effects were suppressed by Did *** increased protein expression of glutamate-L-cysteine ligase catalytic subunit(GCL),heme oxygenase 1(HO-1),and nuclear factor erythroid 2-related factor 2(Nrf2).Besides,Did also induced activation of PI3K/***:These findings indicated Did prevented DOX-induced cardiac injury and apoptosis via activating PI3K/AKT/Nrf2 signaling pathway.

关键词： cardiotoxicity didymin doxorubicin Nrf2 PI3K/Akt

cardiotoxicity of 5-fluorouracil and capecitabine in Chinese patients: a prospective study

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Cancer Communications 2018年第1期38卷 247-253页

作者： Jianjun Peng Chao Dong Chang Wang Weihua Li Hao Yu Min Zhang Qun Zhao Bo Zhu Jun Zhang Wenliang Li Fenghua Wang Qiong Wu Wenhao Zhou Ying Yuan Meng Qiu Gong Chen Center of Gastrointestinal Surgery First Affiliated Hospital of Sun Yat-sen UniversityGuangzhou 510080GuangdongP.R.China Department of the Second Medical Oncology The 3rd Affiliated Hospital of Kunming Medical UniversityYunnan Tumor HospitalKunming 650118YunnanP.R.China Department of Oncology The First Hospital of Jilin UniversityChangchun 130021JilinP.R.China Department of Surgical Oncology Fujian Provincial HospitalFuzhou 350014FujianP.R.China Department of Biological Statistics School of Public HealthNanjing Medical UniversityNanjing 211166JiangsuP.R.China Department of Cardiology Shanghai Jiaotong UniversityShanghai 200030P.R.China The Third Surgery Department the Fourth Hospital of Hebei Medical UniversityTumor Hospital of Hebei ProvinceShijiazhuang 050011HebeiP.R.China Institute of Cancer Xinqiao Hospital of Third Military Medical UniversityChongqing 400037P.R.China Oncology Department Shanghai Ruijin HospitalShanghai 200025P.R.China Oncology Department First Affiliated Hospital of Kunming Medical UniversityKunming 650032YunnanP.R.China Department of Internal Medicine Sun Yat-sen University Cancer CenterGuangzhou 510060GuangdongP.R.China Medical Oncology The first Affiliated Hospital of Bengbu Medical CollegeBengbu 233004AnhuiP.R.China Department of Colorectal Surgery Sun Yat-sen University Cancer Center651 Donfeng RdEastGuangzhou 510060GuangdongP.R.China Medical Oncology The Second Affiliated Hospital of Zhejiang University School of MedicineHangzhou 310009ZhejiangP.R.China Department of Medical Oncology Cancer CenterThe State Key Laboratory of BiotherapyWest China HospitalWest China Medical SchoolSichuan UniversityNo.37Guo Xue XiangChengdu 610041SichuanP.R.China

Background:5-Fluorouracil(5-FU)and capecitabine-associated cardiotoxicity ranging from asymptomatic electro-cardiography(ECG)abnormalities to severe myocardial infarction has been reported in a number of studies,but such cardiotoxicity in Chinese patients with malignant diseases has not been investigated to *** the present study,we aimed to prospectively evaluate the incidence rates and clinical manifestations of 5-FU-and capecitabine-associated cardiotoxicity in cancer patients recruited from multiple centers in ***:Among the 527 patients who completed the study,196 received 5-FU-based chemotherapy and 331 received capecitabine-based chemotherapy as either first-line or adjuvant *** events were reported during the treatment and up to 28 days of *** measures included ECG,myocardial enzymes,cardiac troponin,brain natriuretic peptide and *** analysis and logistic regression were performed for subgroup analysis and identification of significant independent variables that are associated with cardiotoxicity of both ***:In total,161 of 527 patients(30.6%)experienced *** incidence rate of cardiotoxicity was 33.8%(112/331)in the capecitabine group,which was significantly higher than the rate of 25%(49/196)in the 5-FU group(P=0.0042).110/527 patients(20.9%)suffered arrhythmia,105/527(19.9%)developed ischemic changes,while only 20/527 patients(3.8%)presented heart failure and 6/527 patients(1.1%)had myocardial ***-existing cardiac disease,hypertension,capecitabine-based chemotherapy and duration of treatment were identified as sig-nificant risk factors associated with *** odds ratio were 15.7(prior history of cardiac disease versus no history),1.86(capecitabine versus 5-FU),1.06(5-8 versus 1-4 chemotherapy cycles)and 1.58(hypertension versus no hypertension),***:cardiotoxicity induced by fluoropyrimidines in the Chinese population may be und

关键词： 5-Fluorouracil Capecitabine cardiotoxicity