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Effect of CTMP1 gene on pulmonary fibrosis

  • Huonggiang Nguyen (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Uijin Juang (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Suhwan Gwon (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Woohyeong Jung (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Quingzhi Huang (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Soohyeon Lee (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Beomwoo Lee (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • So Hee Kwon (College of Pharmacy, Yonsei Institute of Pharmaceutical Sciences, Yonsei University) ;
  • Seon‑Hwan Kim (Department of Neurosurgery, Institute for Cancer Research, College of Medicine, Chungnam National University) ;
  • Jongsun Park (Department of Pharmacology, College of Medicine, Chungnam National University)
  • Received : 2024.04.14
  • Accepted : 2024.11.13
  • Published : 2025.05.15

Abstract

Protein kinase B (PKB/AKT) is a very important member of the protein kinase family, playing signifcant roles in various crucial processes including insulin-signaling, cell survival, growth, and metabolism. The carboxyl-terminal modulator protein 1 (CTMP1) inhibits PKB, primarily by attenuating its phosphorylation. Idiopathic pulmonary fibrosis (IPF) is an irreversible, chronic, progressive pulmonary disorder; the clinical treatment options are limited. Of the various experimental models, bleomycin-induced lung fibrosis is the most extensively studied. It closely resembles human lung fibrosis. We explored the impact of CTMP1 on bleomycin-induced fibrosis. In vitro experiments involved knockdown of CTMP1 in A549 cells (human alveolar epithelial cells), followed by bleomycin treatment. In vivo, lung fibrosis was induced in mice with ablated CTMP1 via intratracheal bleomycin administration at 2 mg/kg. CTMP1 deletion reduced pulmonary fibrosis and the epithelial-to-mesenchymal transition by inhibiting PKB phosphorylation. These findings suggest that CTMP1 plays a pivotal role in the regulation of lung fibrosis, offering new insights into potential therapeutic approaches for IPF patients.

Keywords

Acknowledgement

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