Development of novel therapeutics targeting mitochondria DNA

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K19387
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Cardiovascular medicine
• Research Institution: Kyushu University
• Principal Investigator: fujino takeo 九州大学, 医学研究院, 助教 (10721904)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: ミトコンドリア / 心不全 / 心筋リモデリング

Outline of Final Research Achievements

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.

Free Research Field

循環器内科学