“…While the origin of airway remodeling is not well understood, a growing body of evidence suggests that airway epithelial cells are a causal factor [ 1 , 2 , 3 , 4 ]. In particular, during asthma exacerbations, airway narrowing causes mechanical compression of airway epithelial cells, which then produce pathologic mediators thereby contributing to airway remodeling [ 5 , 6 , 7 ]. Mechanical compression applied to well-differentiated human bronchial epithelial (HBE) cells activates multiple signaling cascades, including epidermal growth factor receptor (EGFR), protein kinase C (PKC), extracellular signal-regulated kinase (ERK), and transforming growth factor-β (TGF-β) receptor, all of which are linked to a variety of pathophysiologic features of airway remodeling and asthma [ 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 ].…”