- Title
- Epithelial-mesenchymal transition is driven by transcriptional and post transcriptional modulations in copd: implications for disease progression and new therapeutics
- Creator
- Eapen, Mathew Suji; Sharma, Pawan; Gaikwad, Archana Vijay; Lu, Wenying; Myers, Stephen; Hansbro, Philip M.; Sohal, Sukhwinder Singh
- Relation
- International Journal of Chronic Obstructive Pulmonary Disease Vol. 14, p. 1603-1610
- Publisher Link
- http://dx.doi.org/10.2147/COPD.S208428
- Publisher
- Dove Medical Press
- Resource Type
- journal article
- Date
- 2019
- Description
- COPD is a common and highly destructive disease with huge impacts on people and health services throughout the world. It is mainly caused by cigarette smoking though environmental pollution is also significant. There are no current treatments that affect the overall course of COPD; current drugs focus on symptomatic relief and to some extent reducing exacerbation rates. There is an urgent need for in-depth studies of the fundamental pathogenic mechanisms that underpin COPD. This is vital, given the fact that nearly 40%-60% of the small airway and alveolar damage occurs in COPD well before the first measurable changes in lung function are detected. These individuals are also at a high risk of lung cancer. Current COPD research is mostly centered around late disease and/or innate immune activation within the airway lumen, but the actual damage to the airway wall has early onset. COPD is the end result of complex mechanisms, possibly triggered through initial epithelial activation. To change the disease trajectory, it is crucial to understand the mechanisms in the epithelium that are switched on early in smokers. One such mechanism we believe is the process of epithelial to mesenchymal transition. This article highlights the importance of this profound epithelial cell plasticity in COPD and also its regulation. We consider that understanding early changes in COPD will open new windows for therapy.
- Subject
- epithelial-to-mesenchymal transition; EMT; cancer; fibrosis; inflammation; HuR; EGFR; MMP; TGFβ
- Identifier
- http://hdl.handle.net/1959.13/1416849
- Identifier
- uon:37130
- Identifier
- ISSN:1176-9106
- Rights
- This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.
- Language
- eng
- Full Text
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