Development of novel therapeutics targeting mitochondria DNA
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- fujino takeo
- Principal Investigator
- 九州大学
About this project
- Japan Grant Number
- JP15K19387
- Funding Program
- Grants-in-Aid for Scientific Research
- Funding organization
- Japan Society for the Promotion of Science
- Project/Area Number
- 15K19387
- Research Category
- Grant-in-Aid for Young Scientists (B)
- Allocation Type
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- Multi-year Fund
- Review Section / Research Field
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- Biological Sciences > Medicine, Dentistry, and Pharmacy > Clinical internal medicine > Cardiovascular medicine
- Research Institution
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- Kyushu University
- Project Period (FY)
- 2015-04-01 〜 2017-03-31
- Project Status
- Completed
- Budget Amount*help
- 3,900,000 Yen (Direct Cost: 3,000,000 Yen Indirect Cost: 900,000 Yen)
Research Abstract
The purpose of this study was to investigate the mechanism of anti-remodeling effect by mtDNA. We generated volume overload model mice in Twinkle helicase overexpression mice (TW mice) and Tfam overexpression mice (TF mice). TW mice and TF mice increased mtDNA copy number by different mechanism respectively, furthermore each mice suppressed left ventricular remodeling and repressed mitochondrial oxidative stress. However, because oxidative stress were induced in mtDNA, that mtDNA can function as ROS regulatory factor in mitochondria. Furthermore, it was also identified that pressure overload model mice in TW mice and TF mice led to reduction in fibrogenesis and suppression of MMP generation.
Details 詳細情報について
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- CRID
- 1040282256841228800
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- Text Lang
- ja
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- Data Source
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- KAKEN