EMT inhibitor for the treatment of idiopathic pulmonary fibrosis

2017 Fiscal Year Final Research Report

• Project/Area Number: 26461200
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Respiratory organ internal medicine
• Research Institution: Juntendo University
• Principal Investigator: Takahashi Fumiyuki 順天堂大学, 医学部, 准教授 (70327823)
• Co-Investigator(Kenkyū-buntansha): 高橋 和久 順天堂大学, 医学部, 教授 (80245711)
• Co-Investigator(Renkei-kenkyūsha): SAYA Hideyuki 慶応大学, 医学部, 教授 (80264282)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: 特発性肺線維症 / 上皮間葉転換 / 肺胞上皮 / 肺線維症マウスモデル / ブレオマイシン

Outline of Final Research Achievements

It has been reported that transforming growth factor (TGF) β-mediated epithelial-mesenchymal transition (EMT) of alveolar epithelial cells contributes to the pathogenesis of idiopathic pulmonary fibrosis (IPF). However, no agents which can target EMT have not been developed for the treatment of IPF. Here, we established the in vitro models of EMT of alveolar epithelial cells suitable for high-throughput screening of antifibrotic agents for IPF. We found that drug candidate has inhibitory effect on TGF-β-mediated EMT of alveolar epithelial cells in vitro. We also have tested this drug for antifibrotic effect in murine pulmonary fibrosis model induced by bleomycin injection, and found that this drug has antifibrotic activity in vivo. These data suggest that EMT inhibitor may be promising and novel anti-fibrotic agent for the prevention of IPF.

Free Research Field

呼吸器病学