Kidney-Heart crosstalk and mitochondria injury in acute kidney injury
| Project/Area Number |
25461211
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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 | The University of Tokyo |
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Principal Investigator |
Doi Kent 東京大学, 医学部附属病院, 講師 (80505892)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 急性腎障害 / 心腎連関 / ミトコンドリア / 遠隔臓器障害 / 心筋障害 / アポトーシス |
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| Outline of Final Research Achievements |
Acute kidney injury (AKI) is a common complication in critically ill patients treated in intensive care units (ICUs). Cardiorenal syndrome has been defined based on clinical observations that acute and chronic heart failure causes kidney injury and AKI and that chronic kidney disease worsens heart diseases. Possible pathways that connect these two organs have been suggested; however, the precise mechanisms are still unclarified, particularly in AKI-induced cardiac dysfunction. Our animal experiment demonstrated the dysregulation of mitochondrial dynamics caused by an increased Drp1 expression and cellular apoptosis of the heart in a renal ischemia reperfusion model. Although the precise mechanisms that induce cardiac mitochondrial injury in AKI remain unclear, cardiac mitochondria injury will be a novel candidate of drug targets against high mortality in severe AKI.
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Report
(4 results)
Research Products
(2 results)
