Airway remodeling in asthma is characterized by goblet cell hyperplasia, subepithelial fibrosis, and hyperplasia and hypertrophy of airway smooth muscle cells. The airway wall thickness increases because of subepithelial fibrosis, and hyperplasia and hypertrophy of the airway smooth muscle cells and submucosal glands. Airway remodeling, therefore, can often cause irreversible airflow limitation and an increase of airway hyperresponsiveness. Recent studies have described the molecular and cellular mechanisms of collagen deposition in the airway wall such as subepithelial fibrosis. Fibroblasts or myofibroblasts play a critical role in the exaggerated deposition of collagen in asthmatic airways. Bone marrow derived fibroblasts may play a role in fibrotic remodeling in asthmatic airways. Airway remodeling is induced by cytokines and mediators produced in chronic allergic airway inflammation. Since, once formed, remodeling is resistant to asthma therapy, early intervention with inhaled corticosteroid should be considered to prevent the progress of airway remodeling.