2017 Fiscal Year Final Research Report
Biomarkers of cardiac fibrosis in pressure overloaded heart.
Project/Area Number |
15K08190
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General physiology
|
Research Institution | Jikei University School of Medicine |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
南沢 享 東京慈恵会医科大学, 医学部, 教授 (40257332)
岩本 武夫 東京慈恵会医科大学, 医学部, 准教授 (90568891)
|
Research Collaborator |
KUGA Kazuhiro
YAMADA Yuki
USUI Fumio
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Keywords | 線維化 / 圧負荷 |
Outline of Final Research Achievements |
We found that the expression level of FGF23 in cardiac hyptrophy with fibrosis was significantly stronger than that of cardiac hypertrophy without fibrosis. To investigate whether FGF23 was a key factor of cardiac fibrosis, we applied FGF23 on cardiac fibroblast. FGF23 did not show any changes. However, FGF23 tended to promote trans-differentiation of fibroblasts stimulated by TGF-β These results indicate that FGF23 is identified as a novel fibrosis-related gene and may enhance the effect of cytokines (ex TGF-beta) in initiation of cardiac fibrosis.
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Free Research Field |
心筋生理学
|