Document Detail

EMT and interstitial lung disease: a mysterious relationship.
MedLine Citation:
PMID:  22854509     Owner:  NLM     Status:  MEDLINE    
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.
Hidenori Kage; Zea Borok
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Current opinion in pulmonary medicine     Volume:  18     ISSN:  1531-6971     ISO Abbreviation:  Curr Opin Pulm Med     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-08-02     Completed Date:  2012-12-18     Revised Date:  2014-02-17    
Medline Journal Info:
Nlm Unique ID:  9503765     Medline TA:  Curr Opin Pulm Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  517-23     Citation Subset:  IM    
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MeSH Terms
Collagen / metabolism
Endoplasmic Reticulum / physiology
Epithelial-Mesenchymal Transition / physiology*
Fibroblasts / metabolism,  pathology
Lung / pathology
Lung Diseases, Interstitial / pathology*,  physiopathology*
Myofibroblasts / metabolism,  pathology
Grant Support
Reg. No./Substance:

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