| Budget Amount *help |
¥25,350,000 (Direct Cost: ¥19,500,000、Indirect Cost: ¥5,850,000)
Fiscal Year 2015: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2014: ¥8,190,000 (Direct Cost: ¥6,300,000、Indirect Cost: ¥1,890,000)
Fiscal Year 2013: ¥10,790,000 (Direct Cost: ¥8,300,000、Indirect Cost: ¥2,490,000)
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| Outline of Final Research Achievements |
We have previously reported that the accumulation of mitochondrial DNA in cardiomyocytes can induce inflammatory response and heart failure. Mitochondria are usually degraded through mitochondria-specific autophagy, mitophagy. In yeast, Atg32 was found to be an essential molecule during mitophagy, however, no functional homologue for Atg32 in mammalian cells had been identified. In this research we investigated a novel molecular mechanism involved in the mitophagy in mammalian cells, and found BCL2L13 as a functional homologue of Atg32. BCL2L13 induced mitochondrial fragmentation and played an important role as a mitophagic receptor on outer mitochondrial membrane.
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