Development of new therapeutics for kidney diseases by mitochondia-homig drug
| Project/Area Number |
15K08064
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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 |
Medical pharmacy
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| Research Institution | Tohoku University |
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Principal Investigator |
Suzuki Takehiro 東北大学, 医工学研究科, 特任准教授 (50396438)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | ミトコンドリア / 酸化ストレス / ATP / 急性腎障害 / 慢性腎臓病 / 造影剤腎症 / 虚血再灌流 / シスプラチン / 造影剤 / ミトコンドリア病 / mitofilin |
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| Outline of Final Research Achievements |
Mitochondrial dysfunction causes various mitochondrial diseases, kidney injuries and cardiomyopathy. Intracellular ATP depletion and the increasing mitochondria-derived reactive oxygen species (mitROS) are considered as major pathophysiologic mechanisms of disease progression in mitochondrial abnormalities. Recently we reported mitochondria homing drug, mitochonic acid-5 (MA-5) increased intracellular ATP, decreased mitochondrial ROS and improved cell survivals of fibroblasts from mitochondrial disease patients by binding mitochondrial protein Mitofilin and promoting oligomelization of ATP synthases MA-5 improved the renal function and tubular cell injuries in murine renal ischemia reperfusion and cisplatin induced nephropathy models. MA-5 also improved mitochondrial respiratory function in kidney and heart of mitochondrial disease model mice (mitomice).
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Report
(4 results)
Research Products
(53 results)
