Mechanisms responsible for mineralocorticoid receptor-dependent renal injury
| Project/Area Number |
20590253
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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 |
General pharmacology
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| Research Institution | Kagawa University |
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Principal Investigator |
NISHIYAMA Akira Kagawa University, 医学部, 教授 (10325334)
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| Co-Investigator(Kenkyū-buntansha) |
清元 秀泰 香川大学, 医学部附属病院, 講師 (00304585)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2008: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | アルドステロン / ミネラロコルチコイド受容体 / 腎障害 / 糖尿病性腎症 / 薬理学 / 腎臓 / 循環器・高血圧 / 酸化ストレス |
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| Research Abstract |
Possible roles of aldosterone and mineralocorticoid receptor (MR) in the pathphysiology of renal injury have been indicated. We have demonstrated that MR antagonist elicits blood-pressure independent renoprotective effect in type 2 diabetic rats. We also showed that MR is expressed not only in renal distal tubular cells, but also in other renal epithelial and non-epithelial cells including proximal tubular cells, glomerular mesangial cells, podocytes and renal interstitial fibroblasts. Aldosterone induced cell injury through the activation of MAP kinases and reactive oxygen species generation. Treatment with an MR antagonist inhibits renal cell injuries induced by aldosterone. Similar cell injuries were also induced through MR activation by glucocorticoid and high glucose. These observations suggest that locally expressed MR is involved in renal injury through multiple pathways that cannot be simply explained by high aldosterone levels.
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Report
(4 results)
Research Products
(236 results)
