| 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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| 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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