Epithelial-mesenchymal transition in lung development and disease: does it exist and is it important?
- PMID: 24334519
- DOI: 10.1136/thoraxjnl-2013-204608
Epithelial-mesenchymal transition in lung development and disease: does it exist and is it important?
Abstract
Epithelial-mesenchymal transition (EMT) is a process when epithelial cells gradually transform into mesenchymal-like cells losing their epithelial functionality and characteristics. EMT is thought to be involved in the pathogenesis of numerous lung diseases ranging from developmental disorders, fibrotic tissue remodelling to lung cancer. The most important question--namely what is the importance and contribution of EMT in the pathogenesis of several chronic lung conditions (asthma, COPD, bronchiolitis obliterans syndrome and lung fibrosis)--is currently intensely debated. This review gives a brief insight into the mechanism and assessment methods of EMT in various pulmonary diseases and summarises the recent literature highlighting the controversial experimental data and conclusions.
Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
Comment in
-
Importance of epithelial mesenchymal transition (EMT) in COPD and asthma.Thorax. 2014 Aug;69(8):768. doi: 10.1136/thoraxjnl-2014-205582. Epub 2014 May 19. Thorax. 2014. PMID: 24842787 No abstract available.
-
Authors' response: Epithelial-mesenchymal Transition (EMT) is a common molecular programme in epithelial cells which can be triggered by injury.Thorax. 2014 Aug;69(8):769. doi: 10.1136/thoraxjnl-2014-205647. Epub 2014 May 28. Thorax. 2014. PMID: 24870207 No abstract available.
Similar articles
-
The biological role of epithelial-mesenchymal transition in lung cancer (Review).Oncol Rep. 2016 Sep;36(3):1199-206. doi: 10.3892/or.2016.4964. Epub 2016 Jul 21. Oncol Rep. 2016. PMID: 27460444 Review.
-
Epithelial-mesenchymal transition, a spectrum of states: Role in lung development, homeostasis, and disease.Dev Dyn. 2018 Mar;247(3):346-358. doi: 10.1002/dvdy.24541. Epub 2017 Jul 21. Dev Dyn. 2018. PMID: 28646553 Review.
-
Synergistic effects of particulate matter and substrate stiffness on epithelial-to-mesenchymal transition.Res Rep Health Eff Inst. 2014 Nov;(182):3-41. Res Rep Health Eff Inst. 2014. PMID: 25669020
-
Importance of epithelial mesenchymal transition (EMT) in COPD and asthma.Thorax. 2014 Aug;69(8):768. doi: 10.1136/thoraxjnl-2014-205582. Epub 2014 May 19. Thorax. 2014. PMID: 24842787 No abstract available.
-
Authors' response: Epithelial-mesenchymal Transition (EMT) is a common molecular programme in epithelial cells which can be triggered by injury.Thorax. 2014 Aug;69(8):769. doi: 10.1136/thoraxjnl-2014-205647. Epub 2014 May 28. Thorax. 2014. PMID: 24870207 No abstract available.
Cited by
-
Derangement of cell cycle markers in peripheral blood mononuclear cells of asthmatic patients as a reliable biomarker for asthma control.Sci Rep. 2021 Jun 4;11(1):11873. doi: 10.1038/s41598-021-91087-5. Sci Rep. 2021. PMID: 34088958 Free PMC article.
-
Canonical WNT pathway is activated in the airway epithelium in chronic obstructive pulmonary disease.EBioMedicine. 2020 Nov;61:103034. doi: 10.1016/j.ebiom.2020.103034. Epub 2020 Oct 10. EBioMedicine. 2020. PMID: 33045470 Free PMC article.
-
Modeling Molecular Pathogenesis of Idiopathic Pulmonary Fibrosis-Associated Lung Cancer in Mice.Mol Cancer Res. 2024 Mar 1;22(3):295-307. doi: 10.1158/1541-7786.MCR-23-0480. Mol Cancer Res. 2024. PMID: 38015750 Free PMC article.
-
Semaphorin 7a aggravates TGF-β1-induced airway EMT through the FAK/ERK1/2 signaling pathway in asthma.Front Immunol. 2023 Nov 1;14:1167605. doi: 10.3389/fimmu.2023.1167605. eCollection 2023. Front Immunol. 2023. PMID: 38022556 Free PMC article.
-
Long non-coding (lnc)RNA profiling and the role of a key regulator lnc-PNRC2-1 in the transforming growth factor-β1-induced epithelial-mesenchymal transition of CNE1 nasopharyngeal carcinoma cells.J Int Med Res. 2021 Mar;49(3):300060521996515. doi: 10.1177/0300060521996515. J Int Med Res. 2021. PMID: 33752469 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical