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2017 Fiscal Year Final Research Report

Biomarkers of cardiac fibrosis in pressure overloaded heart.

Research Project

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Project/Area Number 15K08190
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field General physiology
Research InstitutionJikei University School of Medicine

Principal Investigator

Kusakari Yoichiro  東京慈恵会医科大学, 医学部, 准教授 (80338889)

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.

Free Research Field

心筋生理学

URL: 

Published: 2019-03-29  

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