Airway remodeling can be defined as changes in the composition, content, and organization of the cellular and molecular constituents of the airway wall. Airway remodeling is a characteristic feature of asthma, and has important functional implications. These structural changes include epithelial detachment, subepithelial fibrosis, increased airway smooth muscle (ASM) mass, decreased distance between epithelium and ASM cells, goblet cell hyperplasia, mucus gland hyperplasia, proliferation of blood vessels and airway edema and changes in the cartilage. Each can contribute to airway hyperreactivity (AHR), and may eventually lead to irreversible airflow obstruction with disease progression. Structural changes can be observed from early onset of the disease and thus remodeling is thought to be characteristic of asthma. Some aspects of airway remodeling can be explained as a consequence of TH2 inflammation, although it has also been suggested that the exaggerated inflammation and remodeling seen in asthmatic airways is the consequence of abnormal injury and repair responses stemming from the susceptibility of bronchial epithelia to components of the inhaled environment. According to this view, remodeling occurs by way of a noninflammatory mechanism, where inflammation of airways and altered structure and function of the airways are parallel and interacting factors. Airway remodeling in established asthma is poorly responsive to current therapies, such as inhalation of corticosteroids and administration of beta(2)-agonists, antileukotrienes, and theophylline.