title: Epithelial and endothelial cell plasticity in chronic obstructive pulmonary disease (COPD).
abstract: Chronic Obstructive Pulmonary Disease (COPD) is mainly caused by smoking and presents with shortness of breath that is progressive and irreversible. It is a worldwide health problem and the fourth most common cause of chronic disability and mortality (even in developed countries). It is a complex disease involving both the airway and lung parenchyma. Small-airway fibrosis is the main contributor to physiological airway dysfunction in COPD. One potential mechanism contributing to small-airway fibrosis is epithelial mesenchymal transition (EMT). When associated with angiogenesis (EMT-type-3), EMT may well also be linked to the development of airway epithelial cancer, which is closely associated with COPD and predominantly observed in large airways. Vascular remodeling has also been widely reported in smokers and patients with COPD but the mechanisms behind it are poorly understood. It is quite possible that the process of endothelial to mesenchymal transition (EndMT) is also active in COPD lungs, in addition to EMT. Understanding these pathological mechanisms will greatly enhance our knowledge of the immunopathology of smoking-related lung disease. Only by understanding these processes can new therapies be developed.
authors.affiliation: School 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. Electronic address: sssohal@utas.edu.au.
authors.forename: Sukhwinder Singh
authors.initials: SS
authors.lastname: Sohal
mesh_terms: D000066670:Cell Plasticity / Q000502:physiology*; D042783:Endothelial Cells; D004847:Epithelial Cells; D058750:Epithelial-Mesenchymal Transition / Q000502:physiology*; D005355:Fibrosis; D006801:Humans; D008168:Lung / Q000473:pathology; D029424:Pulmonary Disease, Chronic Obstructive / Q000209:etiology* / Q000473:pathology*; D012907:Smoking / Q000009:adverse effects; D066253:Vascular Remodeling / Q000502:physiology
keywords: COPD; EMT; EndMT; Fibrosis; Lung cancer