| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Outline of Final Research Achievements |
Apoptosis participates in kidney physiologic remodeling processes and is thought to contribute to pathophysiology of AKI. Understanding the signaling pathways of ROS-induced cell apoptosis would provide important clues to the elucidation of the mechanisms of AKI. One genetic pathway that mediates cell survival or response to ROS stress comprises the sirtuin family. The aim of this study is to understand the protective roles of Sirt1 in AKI. Sirt1 is transcriptionally up-regulated in hypoxic condition in renal tubules, and endogenous Sirt1 maintains cell survival by regulating catalase expression. Sirt1 constitutes a determinant of renal tubular cell apoptosis by regulating cellular ROS levels. The current study therefore unravels both physiological and pathological significance of Sirt1 in ROS-dependent cell survival and apoptosis of renal tubular cells. Furthermore we reported that regulated TxNIP,miR-34a, PNUTS, sestrin2 and BNIP3 play a key role in the pathophysiology of AKI.
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