| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Outline of Final Research Achievements |
Diabetic nephropathy is the leading cause of end stage renal disease. Thus, a new therapeutic strategy to combat the disease is strongly needed. Podocyte damage causes massive proteinuria, leading to rapid decline of renal function. However, the underlying mechanism of the situation is still unknown. It is presumed that the function of an intracellular catabolic mechanism, autophagy-lysosome system, is important for maintaining the survival and function of podocytes because they have poor regeneration capability. In this study, we have revealed that the autophagy-lysosomal system is impaired in podocytes of rats with severe diabetic nephropathy and the activation of lysosomal biosynthesis can reduce apoptosis in the cultured immortalized podocytes stimulated with glucose and lipid toxicity. The activation of autophagy-lysosomal system in podocytes may become a new therapeutic target for diabetic nephropathy.
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