Mitochondrial ROS‐induced ERK1/2 activation and HSF2‐mediated AT 1 R upregulation are required for doxorubicin‐induced cardiotoxicity

Author:

Huang Chih‐Yang1ORCID,Chen Jia‐Yi2,Kuo Chia‐Hua3,Pai Pei‐Ying45,Ho Tsung‐Jung456,Chen Tung‐Sheng27,Tsai Fu‐Jen6,Padma Vijaya V.8,Kuo Wei‐Wen9,Huang Chih‐Yang24510ORCID

Affiliation:

1. Translation Research CoreChina Medical University HospitalTaichungTaiwan

2. Graduate Institute of Basic Medical ScienceChina Medical UniversityTaichung

3. Department of Sports SciencesUniversity of TaipeiTaipeiTaiwan

4. Division of CardiologyChina Medical University HospitalTaichungTaiwan

5. School of Chinese MedicineChina Medical UniversityTaichungTaiwan

6. Chinese Medicine DepartmentChina Medical University Beigang HospitalTaiwan

7. Biomaterials Translational Research CenterChina Medical University HospitalTaichungTaiwan

8. Department of BiotechnologyBharathiar UniversityCoimbatoreIndia

9. Department of Biological Science and TechnologyChina Medical UniversityTaichungTaiwan

10. Department of Health and Nutrition BiotechnologyAsia UniversityTaichung

Funder

China Medical University Hospital

Ministry of Health and Welfare

Ministry of Science and Technology, Taiwan

Publisher

Wiley

Subject

Cell Biology,Clinical Biochemistry,Physiology

Reference58 articles.

1. Captopril ameliorates myocardial and hematological toxicities induced by adriamycin;Al‐Shabanah O.;Biochemistry and Molecular Biology International,1998

2. The cardiotoxicity of chemotherapeutic drugs;Allen A.;Seminars in Oncology,1992

3. Inhibition of DNA Binding by Differential Sumoylation of Heat Shock Factors

4. Angiotensin II type 1 receptor blockers and congestive heart failure;Auer J. W.;Circulation,2001

5. Reactive Oxygen Species Stimulates Receptor Activator of NF-κB Ligand Expression in Osteoblast

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