| Project/Area Number |
24890089
|
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Kidney internal medicine
|
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
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| Project Period (FY) |
2012-08-31 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
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| Keywords | 糖尿病性腎症 / 糸球体上皮細胞 / 腎臓病学 / オートファジー |
|---|
| Research Abstract |
Diabetic nephropathy is a leading cause of end stage of renal disease. Thus new therapeutic strategy is urgently required. Hyperactivation of mTORC1 signal in podocytes has been reported to be strongly associated with the progression of diabetic nephropathy. However, the detailed mechanism underlying diabetes-related mTORC1 activation has remained unclear. In this study, we have revealed that saturated fatty acid is a potent activator of mTORC1 and subsequent inducer of apoptosis in podocytes. Furthermore, autophagy insufficiency related to mTORC1 hayperactivation was strongly associated with the progression of podocyte dysfunction and subsequent proteinuria in mice. The results suggest that inhibition of free fatty acid-mediated mTORC1 activation and activation of autophagy in podocytes are new therapeutic strategies for diabetic nephropathy.
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