Airway and pulmonary fibrosis is a pathological condition associated with chronic airway inflammation. Fibrosis
and architectural remodeling of tissues can severely disrupt lung function, often with fatal consequences. The traditional
paradigm of fibrogenesis is based on the activation of local stromal cells including fibroblasts and their conversion into
myofibroblasts. However, it has become apparent that several airway structural cells, including epithelial cells, endothelial
cells, and pericytes, contribute to lung fibrosis through a process of molecular reprogramming. Recent studies have shown
the important role of epithelial-mesenchymal transition (EMT) in airway diseases and animal models of fibrosis, suggesting
that targeting EMT may be a promising strategy against fibrotic lung disease. In this article, we review the latest advances
on the evidence for EMT in airway diseases, and discuss the underlying mechanisms of EMT and the roles of inflammatory
mediators. We also describe recent patents that could develop into novel therapeutics.
Keywords: Chronic inflammatory airway diseases, EMT, fibrosis, myofibroblast, TGF-β, TNF-α.
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