title: Role of epithelial mesenchymal transition (EMT) in chronic obstructive pulmonary disease (COPD).
abstract: 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 (so called EMT-Type-3) it may well also be the link with the development of cancer, which is closely associated with COPD and predominantly in large airways. In a recent study published in Respiratory Research, Qin Wang and colleagues investigated the role of urokinase plasminogen activator receptor (uPAR) in EMT in small airway epithelium of COPD patients. However, there are some issues with the paper which we wish to comment on.
authors.forename: Sukhwinder Singh
authors.initials: SS
authors.lastname: Sohal
authors.affiliation: NHMRC Centre of Research Excellence for Chronic Respiratory Disease, School of Medicine, University of Tasmania, Hobart 7000, Australia. haydn.walters@utas.edu.au.
authors.forename: Eugene Haydn
authors.initials: EH
authors.lastname: Walters
mesh_terms: D058750:Epithelial-Mesenchymal Transition / Q000276:immunology*; D005260:Female; D006801:Humans; D008168:Lung / Q000276:immunology*; D008297:Male; D029424:Pulmonary Disease, Chronic Obstructive / Q000276:immunology*; D055293:Receptors, Urokinase Plasminogen Activator / Q000276:immunology*; D020545:Respiratory Mucosa / Q000276:immunology*; D012907:Smoking / Q000276:immunology*
chemical_list: D055293:Receptors, Urokinase Plasminogen Activator