| Project/Area Number |
23890085
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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 |
KUME Shinji 滋賀医科大学, 医学部, 特任助教 (00452235)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 慢性腎臓病 / 肥満 / 老化 / 医学 |
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| Research Abstract |
In glomerular diseases, reducing proteinuria is considered as a principal therapeutic target to improve renal outcomes.. Unfortunately, however, some patients develop treatment-resistant proteinuria, resulting in end stage renal disease. In these patients, protecting proximal tubular epithelial cells (PTECs) against proteinuria may be the next therapeutic target to improve renal outcomes. Obesity and aging are independent risk factors for a rapid decline in renal function inpatients with glomerular diseases. Since the severity of proteinuria-induced tubulointerstitial lesions is correlated with renal outcomes, obesity and aging may exacerbate proteinuria-induced tubulointerstitial lesions. If so, identifying the molecular mechanisms underlying obesity- and aging-mediated PTEC vulnerability may lead to new therapy that improves renal outcome in patients with proteinuria. We thus tried to identify a new therapeutic candidate genes by using cDNA microarray analysis in the kidney samples from obese and aged mice with proteinuria. In this study, we have identified a new candidate gene involved in the mechanism underlying obesity- and aging-mediated worsening of proteinuria-induced tubulointerstitial lesion
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