| Project/Area Number |
26461133
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
Miura Tetsuji 札幌医科大学, 医学部, 教授 (90199951)
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| Co-Investigator(Kenkyū-buntansha) |
三木 隆幸 札幌医科大学, 医学部, 准教授 (00336405)
丹野 雅也 札幌医科大学, 医学部, 講師 (00398322)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | mitochondria / cell death / necroptosis / autophagy / signal transduction / ネクロプトーシス / オートファジー / 細胞内情報伝達 / ミトコンドリア |
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| Outline of Final Research Achievements |
This study showed that, in contrast to its role in necrosis, mitochondrial permeability transition (MPT) does not directly trigger cell death in necroptosis of cardiomyocytes and that necroptotic signals significantly inhibit autophagy, which is potentially modulated by MPT, leading to exaggeration of necroptotic cardiomyocyte death. Sequestration of p62 from p62-LC3-II interaction by increased p62-RIP1 interaction and inhibition of fusion of autophagosomes with lysosomes were proposed to be mechanisms by which necroptotic signals inhibits autophagy.
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