Cell Type-specific Role of TGFb Signaling in Cardiac Remodeling and Myocardial Energy Metabolism

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461101
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Cardiovascular medicine
• Research Institution: Gunma University
• Principal Investigator: Koitabashi Norimichi 群馬大学, 医学部附属病院, 助教 (10420093)
• Co-Investigator(Kenkyū-buntansha): KURABAYASHI Masahiko 群馬大学, 医学部附属病院, 教授 (00215047)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 心臓リモデリング / サイトカイン / エネルギー代謝

Outline of Final Research Achievements

Hemodynamic stress induces cardiomyocyte hypertrophy and myocardial fibrosis, resulting pathological cardiac remodeling and heart failure. Myocardial energetics has been shown to be altered in the development of heart failure. How ever, its precise mechanism remains unclear. We hypothesized that TGF-b or BMP7 induced signaling would induce modifications in myocardial energetic abnormality associating with ATP depletion and hypoxic response. We created fibroblast-specific TGFb-receptor deletion model and examined stress-responses in heart. Myocardial fibrosis was inhibited in this model but no significant changes in cardiac function and myocardial energetics. On the other hand, endothelial-specific TGFb receptor deletion model showed no obvious phenotypic difference with control.

Free Research Field

心不全