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EMT and interstitial lung disease a mysterious relationship

EMT and interstitial lung disease a mysterious relationship REVIEW URRENT EMT and interstitial lung disease: a mysterious PINION relationship Hidenori Kage and Zea Borok 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, b-catenin and other transcriptional co-activators at the a-smooth muscle actin (a-SMA) promoter provide direct evidence for crosstalk between transforming growth factor-b (TGFb) and b-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 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Current Opinion in Pulmonary Medicine Wolters Kluwer Health

EMT and interstitial lung disease a mysterious relationship

Borok, Zea
Current Opinion in Pulmonary Medicine , Volume 18 (5) – Sep 1, 2012
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Copyright
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
ISSN
1070-5287
eISSN
1531-6971
DOI
10.1097/MCP.0b013e3283566721
pmid
22854509
Publisher site
See Article on Publisher Site

Abstract

REVIEW URRENT EMT and interstitial lung disease: a mysterious PINION relationship Hidenori Kage and Zea Borok 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, b-catenin and other transcriptional co-activators at the a-smooth muscle actin (a-SMA) promoter provide direct evidence for crosstalk between transforming growth factor-b (TGFb) and b-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

Journal

Current Opinion in Pulmonary Medicine – Wolters Kluwer Health

Published: Sep 1, 2012

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