• Lynne A Murray.
• Respiratory, Inflammation and Autoimmunity, MedImmune Ltd, Granta Park, Cambridge CB21 6GH, UK. MurrayL@MedImmune.com
• Pulm Pharmacol Ther. 2012 Aug 1;25(4):276-80.

AbstractCOPD and IPF are two chronic lung diseases which are characterized by a decline in lung function, resulting in significant morbidity and mortality. Both of these diseases are more commonly associated with an aging population and the duration for which the disease has been underlying is often unknown. Significant matrix deposition occurs, resulting in either non-reversible airways obstruction in the case of COPD and impaired gas exchange and parenchymal consolidation in IPF. There are no approved therapies that have been demonstrated to target these underlying fibrotic changes in the lung. This may in part be due to the challenges of quantitating lung fibrosis in a temporal manner in specific regions of the lung. However, this may also be due to our understanding of aberrant and pathogenic collagen deposition being somewhat limited. The core processes associated with lung fibrosis are often observed in normal wound healing. Moreover, in the extreme fibrotic setting of IPF, the remodelling is sometimes associated with uncontrolled wound healing responses. As wound healing is a critical aspect to maintaining tissue function and homeostasis, targeting this process directly may result in safety concerns. This review therefore describes some of the recent advances in ascertaining pathways promoting lung fibrosis that may be amenable to therapeutic intervention in both COPD and IPF.Copyright © 2011 Elsevier Ltd. All rights reserved.

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