Exploring treatments based on a new understanding of the pathogenesis of pulmonary fibrosis.

2023 Fiscal Year Final Research Report

• Project/Area Number: 21K16118
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 53030:Respiratory medicine-related
• Research Institution: Osaka University
• Principal Investigator: Fukushima Kiyoharu 大阪大学, 免疫学フロンティア研究センター, 特任助教(常勤) (00752156)
• Project Period (FY): 2021-04-01 – 2024-03-31
• Keywords: 肺線維症

Outline of Final Research Achievements

Idiopathic pulmonary fibrosis (IPF) is an incurable disease with a poor prognosis and a strong association with smoking in its pathogenesis. We aim to gain a comprehensive understanding of the pathogenesis of fibrosis by investigating the mechanisms of fibrosis regulation by the RBM7/NEAT1/CXCL12 cascade and the interplay between immune and non-immune cells, as identified in previous studies. The regulatory mechanisms of RBM7 expression were investigated. The novel pathogenesis of fibrotic lesions was investigated by single-cell RNA-seq analysis of lung fibrosis patient samples. Advanced fibrotic lung is considered a devastating end-stage disease, but an active immune response has been shown to maintain fibroblast activation and promote fibrosis. By studying the mechanisms of fibrosis regulation through the interplay between immune and non-immune cells, we have been able to elucidate the molecular and intercellular dynamics that maintain and promote fibrosi

Free Research Field

呼吸器内科学

Academic Significance and Societal Importance of the Research Achievements

今なお根本的な治療薬は開発されておらず、効果的な治療法が不足しているIPFに対して、申請者のグループはSatMやRBM7等の新たな知見を次々に見いだして報告してきており、これらの新知見により肺線維症の発症メカニズムの理解に関して大きな転換がもたらされた。
本研究は、申請者の新知見によりもたらされた肺線維症発症のメカニズムに基づく病態理解をさらに発展させるものであり、社会的にも求められる方向性であり、本研究により線維症を引き起こすメカニズムを新たな視点から理解することが出来るとともに、本研究により新たに見出される知見は更なる新規治療への応用が期待できる。