2013 Fiscal Year Final Research Report
Possible mechanisms responsible for mineralocorticoid-induced renal injury
| Project/Area Number |
23590303
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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 |
General pharmacology
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| Research Institution | Kagawa University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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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 / 老化 |
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| Research Abstract |
There is increasing evidence implicating aldosterone, in addition to angiotensin II, in the pathogenesis of hypertension and renal diseases. We have demonstrated that aldosterone causes renal injury through the activation of MR in aldosterone-infused rats, Dahl salt-sensitive hypertensive rats, but in angiotensin II-infused hypertensive mice. In the kidney, MR is expressed not only in destal tubules, but also in glomerular mesangial cells, podocytes, proximal tubular cells, and fibroblasts. In these cells, MR activation causes cell injury via oxidative stress and senescence. These data suggest that MR blockers provide a potential therapeutic approach for patients with hypertension and renal impairment.
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[Journal Article] Oxidative stress-induced glomerular mineralocorticoid receptor activation limits the benefit of salt reduction in Dahl salt-sensitive rats2012
Author(s)
Kitada K, Nakano D, Liu Y, Fujisawa Y, Hitomi H, Shibayama Y, Shibata H, Nagai Y, Mori H, Masaki T, Kobori H, Nishiyama A
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Journal Title
PLoS ONE
Volume: 7
Pages: e41896
Peer Reviewed
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