Study of reidentification of fibrogenic cells involved in cardiac remodeling and elucidation of molecular control mechanisms

2020 Fiscal Year Final Research Report

• Project/Area Number: 19K23993
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Multi-year Fund
• Review Section: 0903:Organ-based internal medicine and related fields
• Research Institution: Tokai University
• Principal Investigator: YASUDA Jumpei 東海大学, 医学部, 奨励研究員 (90850777)
• Project Period (FY): 2019-08-30 – 2021-03-31
• Keywords: 心不全 / 臓器線維症 / 病態生理学 / 転写因子

Outline of Final Research Achievements

Fibrosis is the excessive accumulation of collagen fibers in organs due to various diseases. Recently, the authors' laboratory revealed that the transcription factor Tcf21 is a regulator of liver fibrosis. It has been suggested that Tcf21 is involved in fibrosis in organs other than the liver. However, the function of Tcf21 in cardiac fibrosis has not been clarified at all. In the present study, we investigated the effects of Tcf21 regulation on the pathogenesis of cardiac fibrosis.
This study demonstrated that the collagen-producing cells in the heart are cardiac fibroblasts, but it did not fully elucidate the function of Tcf21 in cardiac fibroblasts.

Free Research Field

循環薬理学

Academic Significance and Societal Importance of the Research Achievements

冠動脈疾患や高血圧症の患者は増加の一途を辿っており、その発症と進展に伴うコラーゲンの過剰沈着(心臓線維化)は心不全をきたす。心臓線維化を標的とする新たな心不全治療法の開発が喫緊の課題であるが、心臓線維化に関わるコラーゲン産生細胞の由来やその制御機構は不明である。本研究や今後の研究により、Tcf21の発現制御が心臓線維化の病態に及ぼす影響を明らかにすることで、、Tcf21の発現制御による心臓線維化治療という新しい概念の治療法の開発に繋がることが期待される。