| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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)
|
|---|
| Outline of Final Research Achievements |
Mitochondrial dysfunction causes various mitochondrial diseases, kidney injuries and cardiomyopathy. Intracellular ATP depletion and the increasing mitochondria-derived reactive oxygen species (mitROS) are considered as major pathophysiologic mechanisms of disease progression in mitochondrial abnormalities. Recently we reported mitochondria homing drug, mitochonic acid-5 (MA-5) increased intracellular ATP, decreased mitochondrial ROS and improved cell survivals of fibroblasts from mitochondrial disease patients by binding mitochondrial protein Mitofilin and promoting oligomelization of ATP synthases MA-5 improved the renal function and tubular cell injuries in murine renal ischemia reperfusion and cisplatin induced nephropathy models. MA-5 also improved mitochondrial respiratory function in kidney and heart of mitochondrial disease model mice (mitomice).
|
