Fig. 7

Schematic representation of plausible mechanism shows the potential role of GLUT3 in COPD. GLUT3 is positively regulated in bronchial epithelial cells and GLUT3-mediated cigarette smoke induced epithelial-mesenchymal transition by up-regulating the NF-κB/ZEB1 pathway, inducing airway epithelial cells to lose their epithelial characteristics with the loss of polarity and junctional proteins. Airway epithelial cells acquire mesenchymal features such as a spindle shape and to the ability to migrate and secrete matrix proteins. Finally, the extracellular matrix deposition causes airway remodelling, ultimately leading to COPD