Authors
Dodam Moon, Hyomin Park, Tae Yoon Kim, Areum Cha, Youngmin Kim, Jaewon Lee, Joong-Yub Kim, Samina Park, Sung-Hye Park, Jaemoon Koh, Kyongman An, Nam-Joon Cho, Taehoon Kim, Eun Ju Lee, Hyo-Soo Kim
Published in
Molecular therapy : the journal of the American Society of Gene Therapy. Aug 28, 2025. Epub Aug 28, 2025.
Abstract
Transcriptional intermediary factor 1 gamma (TIF1γ) inhibits transforming growth factor-beta (TGFβ) signaling, the main pathway involved in fibrosis. We previously showed that TIF1γ regulated anti fibrotic processes in the liver. Herein, we aimed to evaluate the therapeutic potential of TIF1γ in pulmonary fibrosis (PF). TIF1γ inhibited the TGFβ-induced epithelial-mesenchymal transition in alveolar type 2 cells and activation of fibroblasts in vitro. In activated macrophages, TIF1γ reduced inflammatory cytokine secretion. In the in vivo PF mice model, TIF1γ significantly reduced fibrosis and improved lung function. In ex vivo fibrotic precision cut lung slices from mice and patients with PF, TIF1γ inhibited epithelial-mesenchymal transition of epithelial cells and activation of fibroblasts and reduced inflammatory cytokine secretion in macrophages. Conclusively, TIF1γ is a promising candidate of gene therapy for PF by modulating three cell types (alveolar type 2 cells, fibroblasts, and macrophages) involved in PF pathogenesis.
PMID:
40883987
Bibliographic data and abstract were imported from PubMed on 30 Aug 2025.
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