Role of mitochondrial damage-associated molecule patterns on septic acute kidney injury
| Project/Area Number |
24591194
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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 |
Kidney internal medicine
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
YASUDA Hideo 浜松医科大学, 医学部附属病院, 講師 (60432209)
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| Co-Investigator(Kenkyū-buntansha) |
TSUJI Takayuki 浜松医科大学, 医学部, 助教 (30464126)
KATO Akihiko 浜松医科大学, 医学部附属病院, 准教授 (60324357)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 急性腎障害 / 敗血症 / 自然免疫 / ミトコンドリアDNA / TLR9 |
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| Outline of Final Research Achievements |
The purpose of this study is to clarify whether 1) mitochondrial (mt) DNA is released during sepsis, 2)circulating mtDNA can induce acute kidney injury (AKI), and 3) the effects of mtDNA on kidney injury can be exerted via Toll-like Receptor (TLR) 9. Polymicrobial sepsis by peritonitis in mice early caused lots of circulating mtDNA followed by renal failure. Septic AKI was improved by TLR9 knockout (KO). Admiministration of mt debris including much mtDNA caused renal oxidative stress and mt injury, which was reduced by TLR9KO. Circulating mtDNA released during sepsis contributes to AKI via TLR9.
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Report
(4 results)
Research Products
(3 results)
