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Hepatocyte Growth Factor Deficiency in COPDHepatocyte Growth Factor in COPD: A Mechanism of Emphysema and Small Airway Fibrosis?

Peter J. Barnes, DM, DSc, Master FCCP
Author and Funding Information

From the Airway Disease Section, National Heart & Lung Institute, Imperial College London.

CORRESPONDENCE TO: Peter J. Barnes, DM, DSc, Master FCCP, Airway Disease Section, National Heart & Lung Institute, Dovehouse St, London, SW3 6LY, England; e-mail: p.j.barnes@imperial.ac.uk


FINANCIAL/NONFINANCIAL DISCLOSURES: The author has reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;146(5):1135-1136. doi:10.1378/chest.14-1194
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Hepatocyte growth factor (HGF) (previously known as scatter factor) is a multifunctional cytokine that is secreted by mesenchymal cells, such as fibroblasts, and has effects on epithelial cell growth, morphogenesis, motility, and survival that are mediated by the proto-oncogenic receptor c-Met.1 It plays a key role in the development of organs such as the lung, where it promotes branching of airways and alveolar formation and has been implicated in lung repair.2 Stem cells expressing HGF have been identified in human lung and, by extrapolation from animal studies, are antifibrotic.3 Studies have shown that in mice deficient in c-Met there is a loss of alveolar wall integrity due to loss of alveolar cells, attenuation of the pulmonary vasculature, and an increase in oxidative stress, closely analogous to emphysema. Furthermore, treatment of primary alveolar cells with HGF promotes cell survival and enhanced production of antioxidants.4 Fibroblasts cultured from emphysematous lung produce less HGF than normal and it has been implicated in impaired alveolar repair in emphysema.5 With this background, it is surprising that so little attention has been paid to the role of HGF in COPD. However, in this issue of CHEST (see page 1159), Kanazawa et al,6 in a clinical study from Japan, show convincing evidence for reduced secretion of HGF in peripheral lung of patients with COPD compared with age-matched normal smokers and healthy control subjects and that this is correlated with disease severity and reduced gas transfer. This is consistent with a reduction in HGF having a role in emphysema, and, indeed, there is also a correlation between reduced HGF concentrations and low attenuation areas (emphysema) on the CT scan.

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