| Co-Investigator(Kenkyū-buntansha) |
MAKITA Naomasa 北海道大学, 大学院・医学研究科, 准教授 (00312356)
KINUGAWA Shintaro 北海道大学, 大学院・医学研究科, 講師 (60399871)
MATSUI Yutaka 北海道大学, 遺伝子病制御研究所, 特任准教授 (30431381)
ISHIMORI Naoki 北海道大学, 大学院・医学研究科, 助教 (70399848)
HATAKEYAMA Shigetsugu 北海道大学, 大学院・医学研究科, 教授 (70294973)
|
|---|
| Budget Amount *help |
¥111,540,000 (Direct Cost: ¥85,800,000、Indirect Cost: ¥25,740,000)
Fiscal Year 2012: ¥21,320,000 (Direct Cost: ¥16,400,000、Indirect Cost: ¥4,920,000)
Fiscal Year 2011: ¥21,320,000 (Direct Cost: ¥16,400,000、Indirect Cost: ¥4,920,000)
Fiscal Year 2010: ¥22,100,000 (Direct Cost: ¥17,000,000、Indirect Cost: ¥5,100,000)
Fiscal Year 2009: ¥22,100,000 (Direct Cost: ¥17,000,000、Indirect Cost: ¥5,100,000)
Fiscal Year 2008: ¥24,700,000 (Direct Cost: ¥19,000,000、Indirect Cost: ¥5,700,000)
|
|---|
| Research Abstract |
The role of mitochondria in maintaining the biological function is dynamically regulated by mitochondrial DNA (mtDNA), a closed-circular double-stranded DNA molecule of～16.5 kb. MtDNA decline, mitochondrial defects, and mitochondrial oxidative stress are now well recognized in a variety of diseases such as neurodegenerative diseases, diabetes mellitus, cancer, and even aging. The present study clarified the crucial role of mitochondrial transcription factor A (TFAM) in cardiovascular stress response. With further knowledge on the mechanisms of TFAM for maintenance of mtDNA copy number and mitochondrial function, it may eventually be possible to develop novel strategies for the treatment ofcardiovascular diseases including heart failure.
|
