2015 Fiscal Year Final Research Report
Strategy for the personalized CKD medicine based on the crosstalk between albumin-bound uremic toxin and kidney
Project/Area Number |
25460190
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Medical pharmacy
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Research Institution | Kumamoto University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
MARUYAMA Toru 熊本大学, 薬学部, 教授 (90423657)
OTAGIRI MASAKI 崇城大学, 薬学部, 教授 (80120145)
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Keywords | 尿毒素 / 腎障害 / 心血管障害 / 酸化ストレス |
Outline of Final Research Achievements |
Chronic kidney disease (CKD), marked by a progressive loss in renal function, is a leading cause of hemodialysis initiation and cardiovascular disease (CVD). Understanding the molecular mechanism responsible for the progression of CKD and cardiovascular damage regarding crosstalk between the kidney and cardiovascular system is an important issue in controlling the pathogenesis of CKD-CVD. However, the mechanisms involved in CKD-CVD are not well understood. We have been investigating the role of protein-bound uremic toxins, that are difficult to remove by hemodialysis, on the onset and progression of CKD and CVD. Here, we focus on two sulfate conjugated uremic toxins, namely, indoxyl sulfate (IS) and p-cresyl sulfate (PCS), and summarize recent studies that provide new insights on the molecular mechanisms responsible for uremic toxin-induced oxidative tissue damage via a cardiovascular-renal connection.
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Free Research Field |
医療薬学
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