2016 Fiscal Year Final Research Report
The role of mitoNEET on the regulation of mitochondrial function in skeletal muscle failure
Project/Area Number |
26350879
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Applied health science
|
Research Institution | Hokkaido University |
Principal Investigator |
|
Research Collaborator |
FURIHATA Takaaki
TAKADA Shingo
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Keywords | ミトコンドリア / 骨格筋不全 / 鉄代謝 |
Outline of Final Research Achievements |
In various chronic disease model mice, exercise capacity was reduced, skeletal muscle abnormalities such as mitochondrial dysfunction in the skeletal muscle and fiber type switch occurred, iron content within mitochondria was increased, and oxidative stress was enhanced. In mice deleted mitoNEET, we newly created, iron content within mitochondria was increased, oxidative stress was enhanced, and mitochondrial morphology and function was impaired, which resulted in the reduced exercise capacity. There were no differences in the known protein associated with iron homeostasis in mitochondria. In the analysis by protein interaction, we found that mitoNEET combined with cytosolic protein X associated with iron homeostasis and mitochondrial inner membrane protein Y associated with transportation of some substances into mitochondria.
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Free Research Field |
運動生理
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