2016 Fiscal Year Final Research Report
Development of treatment for cardiac impairment in CD36 deficiency with using iPS cell
Project/Area Number |
15K21139
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Cardiovascular medicine
Metabolomics
|
Research Institution | Osaka University |
Principal Investigator |
|
Research Collaborator |
KOBAYASHI Takuya
SAGA Ayami
|
Project Period (FY) |
2015-04-01 – 2017-03-31
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Keywords | 心筋エネルギー代謝 / 長鎖脂肪酸 / グルコース / CD36 / 圧負荷 / iPS細胞 |
Outline of Final Research Achievements |
(1) Investigation of CD36KO mice hearts under pressure overload condition: CD36KO mice heart showed impaired tolerance of pressure overload with decreased ATP concentration in the heart, eccentric hypertrophic change, and accelerated fibrotic change. These findings suggest that fatty acid uptake through CD36 in the heart is essential to maintenance cardiac energy provision, cardiac function and histological structure under pressure overload. We are submitting these results for the scientific paper. (2) The analyses with using the cardiomyocytes differentiated from iPS cell lines derived from T lymphocytes donated from the patients: Although we tried to analyze the characteristics of cardiomyocytes from iPS cell lines donated from control patients and CD36 deficient patients, the results were not reproducible. We are exploring the methods.
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Free Research Field |
循環器内科
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