| Budget Amount *help |
¥25,610,000 (Direct Cost: ¥19,700,000、Indirect Cost: ¥5,910,000)
Fiscal Year 2019: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2018: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2017: ¥13,520,000 (Direct Cost: ¥10,400,000、Indirect Cost: ¥3,120,000)
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| Outline of Final Research Achievements |
The aim of this research is to characterize the role of hypoxia signaling in cardiomyocyte cell cycle regulation. Firstly, we found that mitochondrial metabolism plays critical roles in cardiomyocyte cell cycle arrest in the postnatal heart. Secondly, in order to determine the roles of hypoxia signaling in proliferative cardiomyocytes in the adult heart, we utilized conditional knock-in and knock-out mouse model and found that hypoxia inducible factor 1 alpha (hif1a) and amelioration of oxidative stress are both critical for maintenance of cardiomyocyte turnover in the adult heart. Our research provides a unique insight into mechanisms underlying cardiomyocyte cell cycle, and may pave the way to induce cardiomyocyte proliferation in the human infarcted heart.
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