Abstract
Unfortunately, the research effort directed into chronic obstructive pulmonary disease (COPD) has been disproportionately weak compared to its social importance, and indeed it is the least researched of all common chronic conditions. Tobacco smoking is the major etiological factor. Only 25% of smokers will develop “classic” COPD; in these vulnerable individuals the progression of airways disease to symptomatic COPD occurs over two or more decades. We know surprisingly little about the pathobiology of COPD airway disease, though small airway fibrosis and obliteration are likely to be the main contributors to physiological airway dysfunction and these features occur earlier than any subsequent development of emphysema. One potential mechanism contributing to small airway fibrosis/obliteration and change in extracellular matrix (ECM) is epithelial mesenchymal transition (EMT), so called Type-II EMT. When associated with angiogenesis (Type-III EMT) it may well also be a link with the development of lung (airway) cancer which is closely associated with COPD. Active EMT in COPD may help to explain why lung cancer is so common in smokers and also the core pathophysiology of small airway fibrosis. Better understanding may lead to new markers for incipient neoplasia, and better preventive management of patients. There is serious need to understand key components of airway EMT in smokers and COPD, and to demarcate novel drug targets for the prevention of lung cancer and airway fibrosis, as well as better secondary management of COPD. Since over 90% of human cancer arises in epithelia and the involvement of EMT in all of these may be a central paradigm, insights gained in COPD may have important generalizable value.
Highlights
We recently published that Epithelial mesenchymal transition (EMT) is an active process in large airways of chronic obstructive pulmonary disease (COPD) patients [17,18]
More importantly which proteins/pathways are amendable to current therapeutics and which will require new modalities of interaction are not clearly understood. In this editorial we will focus on recent advances made in evidence of active processes of EMT in airway disease and its potential clinical importance especially in COPD, and with the use of analysis of what we know from other organ disease processes
The reticular basement membrane (Rbm) in large airways is hyper-vascular [14,15,16] i.e. give the appearance of active EMT type-III, and it is the large airways in COPD, where cancer formation is common, especially squamous cell carcinoma [1,6,7]
Summary
Epithelial mesenchymal transition (EMT) is a process in which epithelial cells undergo a transition to a motile mesenchymal phenotype [1]. There are two subsequent outcome possibilities with active EMT: severe and even complete organ fibrosis (Type II EMT), development of a premalignant stroma when associated with angiogenesis (Type III EMT) [1,7,8,9,10,11,12,13,14,15,16] This complex process of EMT involves essential changes in a wide range of proteins gained, maintained or attenuated [13], but most of the studies reported in the literature have been able to focus on only a few specific markers and are likely to be far from complete. In this editorial we will focus on recent advances made in evidence of active processes of EMT in airway disease and its potential clinical importance especially in COPD, and with the use of analysis of what we know from other organ disease processes
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