| Budget Amount *help |
¥42,510,000 (Direct Cost: ¥32,700,000、Indirect Cost: ¥9,810,000)
Fiscal Year 2016: ¥7,930,000 (Direct Cost: ¥6,100,000、Indirect Cost: ¥1,830,000)
Fiscal Year 2015: ¥7,930,000 (Direct Cost: ¥6,100,000、Indirect Cost: ¥1,830,000)
Fiscal Year 2014: ¥26,650,000 (Direct Cost: ¥20,500,000、Indirect Cost: ¥6,150,000)
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| Outline of Final Research Achievements |
We defined chronic kidney disease based on the diabetes, obesity, and hypertension as metabolic kidney disease and found the molecular mechanism. We delineated the pathological relevance of iNAMPT of proximal tubular cells. The expression of iNAMPT was reduced by TGFb in diabetic kidney disease. We also analyzed regulatory mechanism for the promoter activity of iNMPT genes. In diabetic kidney disease, iNAMPT expression was downregulated which contributed to the tissue fibrotic changes through the reduced expressions of Sirt6. We also investigated the role of NMMT in the pathogenesis of tissue fibrotic changes of both kidney and liver. NMMT-overexpressing mice exhibited prominent liver fibrosis but not renal fibrosis. Liver fibrosis was demonstrated to result from the decreased turnover of methionine metabolism, which lead to methyl-donor deficiency and epigenetic induction of CTGF gene in the liver.
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