| Budget Amount *help |
¥18,590,000 (Direct Cost: ¥14,300,000、Indirect Cost: ¥4,290,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2012: ¥13,390,000 (Direct Cost: ¥10,300,000、Indirect Cost: ¥3,090,000)
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| Outline of Final Research Achievements |
The lower proteolytic capability of autophagy was observed in the liver from NAFLD patients. Liver injury and hepatic inflammation correlate with autophagic dysfunction in non-alcoholic fatty liver disease (NAFLD). These findings indicate that the suppression of autophagic proteolysis by hepatic steatosis is involved in the pathogenesis of NAFLD. Impairment of autophagic proteolysis is caused by alteration of lysosomal proteins. Changes in lysosomal proteins due to hepatic steatosis might disturb autophagosomal acidification and proteolytic activity. Interestingly, autophagic dysfunction and suppression of cathepsin L expression observed in NAFLD lead to the production of anti-oxidant molecules and accelerate liver regeneration. Our results from this study may provide new approaches for the prediction of prognosis, prevention and treatment of NAFLD.
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