| Budget Amount *help |
¥44,980,000 (Direct Cost: ¥34,600,000、Indirect Cost: ¥10,380,000)
Fiscal Year 2015: ¥13,390,000 (Direct Cost: ¥10,300,000、Indirect Cost: ¥3,090,000)
Fiscal Year 2014: ¥14,300,000 (Direct Cost: ¥11,000,000、Indirect Cost: ¥3,300,000)
Fiscal Year 2013: ¥17,290,000 (Direct Cost: ¥13,300,000、Indirect Cost: ¥3,990,000)
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| Outline of Final Research Achievements |
Chronic kidney disease (CKD) increases the disease risk of liver as well as that of kidney. However, the mechanisms remain unclear. In the present study, an increase of plasma transforming growth factor-β1 (TGF-β1) in 5/6 nephrectomy (5/6Nx) mice led to the decreased expression of the Dbp gene, controlling the function of cytochrome P450 (CYPs). Cyp3a11 and Cyp26a1, encoding key proteins in retinol metabolism, decreased in 5/6Nx mice. The accumulation of serum retinol induced renal apoptosis in 5/6Nx mice. The alterations of retinol metabolism and renal dysfunction in 5/6Nx mice were decreased by an anti-TGF-β1 antibody.The present study suggests that the chronic renal failure in 5/6Nx mice causes the inflammation by the abnormal signal transduction in high TGF-βexpression from the kidney and decrease the function of CYPs in liver. Finally, the cell cycle regulatory factor in kidney plays an important role of CKD and may be a promising therapeutic target in the treatment of CKD.
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