Related Experiment Video
Updated: May 19, 2026

Monitoring Lung Function with Electrical Impedance Tomography in the Intensive Care Unit
Published on: September 6, 2024
EMT and interstitial lung disease: a mysterious relationship
1Will Rogers Institute Pulmonary Research Center, Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Southern California, Los Angeles, California, USA.
Purpose Of Review:
Pathogenesis of interstitial lung diseases (ILD) has largely been investigated in the context of the most frequent ILD, idiopathic pulmonary fibrosis (IPF). We review studies of epithelial-to-mesenchymal transition (EMT) and discuss its potential contribution to collagen-producing (myo)fibroblasts in IPF.
Recent Findings:
Endoplasmic reticulum (ER) stress leading to epithelial apoptosis has been reported as a potential etiologic factor in fibrosis. Recent studies further suggest EMT as a link between ER stress and fibrosis. Combinatorial interactions among Smad3, β-catenin and other transcriptional co-activators at the α-smooth muscle actin (α-SMA) promoter provide direct evidence for crosstalk between transforming growth factor-β (TGFβ) and β-catenin pathways during EMT. Lineage tracing yielded conflicting results, with two recent studies supporting and one opposing a role for EMT in lung fibrosis.
Summary:
Advances have been made in elucidating causes and mechanisms of EMT, potentially leading to new treatment options, although contributions of EMT to lung fibrosis in vivo remain controversial. In addition to EMT providing a direct source of (myo)fibroblasts, expression of mesenchymal markers may reflect epithelial injury, in which case inhibition of EMT might be deleterious. EMT-derived cells may also contribute to aberrant epithelial-mesenchymal crosstalk that promotes fibrogenesis.
Related Concept Videos
Pulmonary Embolism I: Introduction
Pulmonary Embolism I: Introduction
Atelectasis II: Pathophysiology
Chronic Obstructive Pulmonary Disease II: Emphysema
Pulmonary Edema II: Pathophysiology
Chronic Obstructive Pulmonary Disease-II: Pathophysiology
Chronic Inflammation
