What are the differences between statin and the shortage of cellular cholesterol content in the pathology of rhabdomyolysis ?
| Project/Area Number |
24659440
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Metabolomics
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
MATSUZAKA Takashi 筑波大学, 医学医療系, 准教授 (70400679)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | コレステロール代謝 / 骨格筋 / 脂質代謝 / 横紋筋融解症 |
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| Research Abstract |
Statin is an inhibitor for HMGCR, which is a rate-limiting enzyme for cholesterol synthesis. Although statin is an effective drug for hypercholesterolemia, statin develops rhabdomyolysis as a side effect. To understand the mechanism of the pathogenesis of rhabdomyolysis by statin, we generated the skeletal muscle-specific HMGCR knockout mice. These mice showed the same phenotypes as rhabdomyolysis. We found that the removal of the insufficient mitochondria by autophagy was dysregulated in skeletal muscle of these mice. Next, we will determine the mechanism that mitochondria function and autophagy are dysfunctioned in skeletal muscle of HMGCR knockout mice.
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Report
(3 results)
Research Products
(5 results)
