| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Outline of Final Research Achievements |
Although cardiac reverse remodeling involving regression of cardiac hypertrophy occurs after control of etiological factors, the molecular mechanisms remain to be clarified. We hypothesized that autophagic degradation of mitochondria and mitochondrial fusion/fission play an important role during reverse remodeling. We identified Bcl2-L-13 as a mitophagy receptor on outer mitochondrial membrane. Bcl2-L-13 binds to LC3 through the WXXI motif and induces mitochondrial fragmentation and mitophagy not only in HEK293 cells but in rat neonatal cardiomyocytes. The BH domains are important for the fragmentation, while the WXXI motif facilitates mitophagy. Rubicon is thought to negatively regulate autophagic machinery. We generated cardiac-specific deficient mice of Bcl2-L-13 and Rubicon.
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