Related Experiment Video

Updated: May 10, 2025

Phenotyping Mouse Pulmonary Function In Vivo with the Lung Diffusing Capacity
07:13

Phenotyping Mouse Pulmonary Function In Vivo with the Lung Diffusing Capacity

Published on: January 6, 2015

10.5K

Effect of CTMP1 gene on pulmonary fibrosis

Huonggiang Nguyen1,2, Uijin Juang1,2, Suhwan Gwon1,2

  • 1Department of Pharmacology, College of Medicine, Chungnam National University, Daejeon, 35015 Republic of Korea.

Toxicological Research
|April 28, 2025
PubMed

Insights

Carboxyl-terminal modulator protein 1 (CTMP1) deletion reduces lung fibrosis by inhibiting protein kinase B (PKB/AKT) phosphorylation. This suggests CTMP1 is a key regulator in pulmonary fibrosis, offering potential therapeutic targets for idiopathic pulmonary fibrosis (IPF).

Area of Science:

  • Cellular Biology
  • Pulmonary Medicine
  • Biochemistry

Background:

  • Protein kinase B (PKB/AKT) is crucial for cell survival, growth, and metabolism.
  • Carboxyl-terminal modulator protein 1 (CTMP1) negatively regulates PKB/AKT activity.
  • Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with limited treatment options.

Purpose of the Study:

  • To investigate the role of CTMP1 in the pathogenesis of bleomycin-induced lung fibrosis.
  • To determine if CTMP1 influences the epithelial-to-mesenchymal transition (EMT) in lung fibrosis.
  • To explore CTMP1 as a potential therapeutic target for IPF.

Main Methods:

  • In vitro: CTMP1 knockdown in A549 human alveolar epithelial cells followed by bleomycin treatment.
  • In vivo: Lung fibrosis induction in CTMP1-ablated mice using intratracheal bleomycin.
  • Assessment of pulmonary fibrosis and PKB/AKT phosphorylation levels.

Main Results:

  • CTMP1 deletion significantly reduced pulmonary fibrosis in mice.
  • CTMP1 knockdown inhibited bleomycin-induced epithelial-to-mesenchymal transition (EMT) in A549 cells.
  • Reduced PKB/AKT phosphorylation was observed in CTMP1-ablated models.

Conclusions:

  • CTMP1 plays a critical role in regulating lung fibrosis development.
  • Inhibition of CTMP1 attenuates lung fibrosis and EMT by modulating PKB/AKT signaling.
  • Targeting CTMP1 may offer a novel therapeutic strategy for idiopathic pulmonary fibrosis (IPF).
Keywords:
CTMP1EMTIPFLung fibrosisPKB

More Related Videos

A Multimodal Imaging Approach Based on Micro-CT and Fluorescence Molecular Tomography for Longitudinal Assessment of Bleomycin-Induced Lung Fibrosis in Mice07:38

A Multimodal Imaging Approach Based on Micro-CT and Fluorescence Molecular Tomography for Longitudinal Assessment of Bleomycin-Induced Lung Fibrosis in Mice

Published on: April 13, 2018

11.4K
Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin10:21

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Published on: September 12, 2019

6.9K

Related Concept Videos

Cystic Fibrosis: Pathogenesis01:23

Cystic Fibrosis: Pathogenesis

Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
136
Cystic Fibrosis: Management01:24

Cystic Fibrosis: Management

Cystic fibrosis (CF) is an autosomal recessive disorder that predominantly affects individuals of Northern European descent, occurring at a rate of 1 in 3500. It is caused by a genetic mutation in a gene on chromosome 7, most commonly the ΔF508 mutation, that codes for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. This results in thicker mucus secretions and obstruction pathologies in multiple organs, including the lungs and sinuses.
Sinus disease and chronic...
94