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Published on: June 14, 2022
Epithelial and endothelial cell plasticity in chronic obstructive pulmonary disease (COPD)
1School of Health Sciences, Faculty of Health, University of Tasmania, Locked Bag - 1322, Newnham Drive, Launceston, Tasmania 7248, Australia; NHMRC Centre of Research Excellence for Chronic Respiratory Disease, University of Tasmania, Hobart, Tasmania 7000, Australia.
Chronic Obstructive Pulmonary Disease (COPD) involves progressive shortness of breath due to smoking. Understanding epithelial and endothelial mesenchymal transitions in COPD may lead to new therapies for this complex lung disease.
Area of Science:
- Pulmonary Medicine
- Cell Biology
- Pathology
Background:
- Chronic Obstructive Pulmonary Disease (COPD) is a major global health issue, characterized by progressive, irreversible shortness of breath, primarily caused by smoking.
- COPD is a complex lung disease affecting airways and parenchyma, with small-airway fibrosis significantly contributing to dysfunction.
- Small-airway fibrosis and vascular remodeling are key pathological features in COPD, but their underlying mechanisms require further elucidation.
Purpose of the Study:
- To explore the role of epithelial mesenchymal transition (EMT) in small-airway fibrosis and its potential link to airway epithelial cancer in COPD.
- To investigate the possible involvement of endothelial to mesenchymal transition (EndMT) in vascular remodeling observed in COPD lungs.
- To enhance understanding of the immunopathology of smoking-related lung diseases and identify targets for novel therapies.
Main Methods:
- Review of existing literature on COPD pathogenesis, focusing on cellular mechanisms like EMT and EndMT.
- Analysis of pathological findings in small airways and lung parenchyma related to fibrosis and vascular remodeling.
- Correlation of EMT and EndMT processes with smoking history and disease severity in COPD patients.
Main Results:
- Epithelial mesenchymal transition (EMT) is a potential mechanism driving small-airway fibrosis in COPD.
- EMT, particularly EMT-type-3 associated with angiogenesis, may contribute to airway epithelial cancer development in COPD patients.
- Endothelial to mesenchymal transition (EndMT) is hypothesized to play a role in the vascular remodeling seen in COPD lungs.
Conclusions:
- Understanding EMT and EndMT pathways is crucial for comprehending the immunopathology of smoking-related lung diseases like COPD.
- Elucidating these cellular transitions can pave the way for the development of innovative therapeutic strategies for COPD.
- Further research into EMT and EndMT mechanisms is essential for advancing COPD treatment and management.
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