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Updated: Jun 7, 2026
06:02
Development of an In Vitro Assay to Evaluate Contractile Function of Mesenchymal Cells that Underwent Epithelial-Mesenchymal Transition
Published on: June 10, 2016
Epithelial-mesenchymal interactions in pulmonary fibrosis
1Department of Medicine, Cardiovascular Research Institute, University of California, San Francisco, 94143, USA. hal.chapman@ucsf.edu
Annual Review of Physiology
|November 9, 2010
Summary
Lung epithelial cells undergo epithelial-mesenchymal transition (EMT) in response to injury and inflammation. Understanding TGFβ1 signaling in EMT could lead to therapies for fibrotic lung diseases.
Area of Science:
- Cell Biology
- Pulmonary Medicine
- Pathology
Background:
- Lung epithelial cells are central to lung injury, repair, and fibrotic diseases.
- Epithelial-mesenchymal transition (EMT) is a key cellular response to microenvironmental cues.
- EMT is a reversible process where epithelial cells gain mesenchymal traits and signaling capacity.
Purpose of the Study:
- To elucidate the signaling mechanisms coordinating TGFβ1 activity with inflammation and injury in lung epithelial cells.
- To understand how repeated injury and inflammation disrupt normal repair pathways.
- To identify therapeutic targets for fibrotic lung diseases by understanding EMT regulation.
Main Methods:
- Investigated integrin-sensing systems.
- Analyzed the coordination of TGFβ1 signaling with inflammatory signals and cell injury.
- Examined the impact of repeated injury, inflammation, and hypoxia on repair pathways.
Main Results:
- Distinct integrin-sensing systems coordinate TGFβ1, inflammation, and injury.
- Repeated injury leads to persistent inflammation and hypoxia, disrupting repair.
- These factors can overwhelm repair, promoting sustained fibrogenesis.
Conclusions:
- Understanding TGFβ1-driven mesenchymal responses is crucial for treating fibrotic lung diseases.
- Targeting specific signaling mechanisms may attenuate fibrogenesis while preserving TGFβ1's homeostatic functions.
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