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A Doxorubicin-induced Cardiomyopathy Model in Adult Zebrafish
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UVRAG Deficiency Exacerbates Doxorubicin-Induced Cardiotoxicity
Lin An1, Xiao-Wen Hu1, Shasha Zhang1
1Bio-X-Renji Hospital Research Center, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Scientific Reports
|February 23, 2017
Summary
Ultra-violet radiation resistance-associated gene (UVRAG) deficiency worsens chemotherapy drug Doxorubicin (DOX)-induced heart damage by impairing autophagy. Intermittent fasting may protect against this cardiotoxicity.
Area of Science:
- Cardiology
- Oncology
- Molecular Biology
Background:
- Doxorubicin (DOX) is a vital chemotherapy agent but causes cardiotoxicity.
- Ultra-violet radiation resistance-associated gene (UVRAG) is crucial for maintaining cardiac autophagic flux.
- The role of UVRAG in DOX-induced cardiotoxicity requires elucidation.
Purpose of the Study:
- To investigate the role of UVRAG-mediated autophagy in Doxorubicin-induced cardiotoxicity.
- To explore intermittent fasting as a potential intervention for DOX cardiotoxicity.
Main Methods:
- Established mouse models of acute and chronic DOX-induced cardiotoxicity.
- Assessed cardiac function, histology, apoptosis, and reactive oxygen species (ROS) levels.
- Evaluated autophagic flux and the impact of UVRAG deficiency and intermittent fasting.
Main Results:
- UVRAG deficiency exacerbated DOX-induced mortality and cardiotoxicity, including cardiac dysfunction, apoptosis, and fibrosis.
- DOX treatment impaired autophagic flux, an effect worsened by UVRAG deficiency.
- Intermittent fasting restored autophagic flux and ameliorated DOX-induced pathological changes.
Conclusions:
- UVRAG deficiency exacerbates DOX cardiotoxicity by aggravating impaired autophagic flux.
- Intermittent fasting shows potential as a therapeutic strategy to mitigate DOX-induced cardiotoxicity by restoring autophagic flux.
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