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 airway epithelial cancer, which is closely associated with COPD and predominantly in large airways. In a recent study published in Respiratory Research, Reimann and colleagues, showed increased expression of S100A4 in vasculature of human COPD and murine lungs. It is quite possible that the process of endothelial to mesenchymal transition (EndMT) is active in COPD lungs which we wish to comment on.