| Project/Area Number |
22590890
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Osaka University |
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Principal Investigator |
KITAMURA Harumi 大阪大学, 大学院・医学系研究科, 特任助教 (60570356)
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| Co-Investigator(Kenkyū-buntansha) |
ISAKA Yoshitaka 大阪大学, 大学院・医学系研究科, 准教授 (00379166)
TAKABATAKE Yoshitsugu 大阪大学, 大学院・医学系研究科, 助教 (30403075)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | オートファジー / シスプラチン / タンパク凝集体 / 虚血再還流 / 近位尿細管 / ミトコンドリア / クロロキン / シクロスポリン / 代謝ストレス / シスプラチン腎症 / 虚血再還流傷害 / p62 / LC3 / 細胞内封入体 |
|---|
| Research Abstract |
In kidney, proximal tubules consume a large amount of energy in the process of electrolyte reabsorption. These tubules contain large quantities of mitochondria which provide the energy for this reabsorption. Proximal tubules are susceptible to many kinds of insults such as ischemia-reperfusion injury and nephrotoxic substrates, but little is known of the factors that counteract cellular stress signaling pathways. Autophagy mediates bulk degradation and recycling of cytoplasmic constituents to maintain cellular homeostasis. We demonstrated the critical role of autophagy in normal proximal tubule function and protection against acute tubular injury including ischemia-reperfusion injury and cisplatin nephrotoxicity.
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