Remodeling in asthma and chronic obstructive pulmonary disease

Airway and lung tissue remodeling and fibrosis play an important role in the development of symptoms associated with lung function loss in asthma and chronic obstructive pulmonary disease (COPD). In the past decades, much attention has been paid to the inflammatory cellular process involved in airway remodeling in these two diseases. However, it is increasingly clear that resident cells contribute to airway and lung tissue remodeling and to associated fibrosis as well. This article deals with some new aspects and discusses the role of vasculature and vascular endothelial growth factor in the development of airway obstruction and airway wall fibrosis in asthma and COPD. Moreover, it addresses the extracellular matrix (ECM) turnover as present in both asthma and COPD. All components of lung ECM (collagen, elastic fibers, proteoglycans) have been shown to be potentially altered in these two diseases. Finally, the interaction between transforming growth factor (TGF), Smad signaling, and TGF in the ECM turnover will be discussed. We propose that ECM damage and repair contribute to airway and lung tissue pathology and that the vasculature may enhance this process. The localization of this process is dependent on the etiology of the disease (i.e., allergen-driven in asthma and smoke-driven in COPD) and the local environment in which the pathologic process takes place