Asthma represents a chronic inflammatory process of the airways followed by healing whose end result may be an altered structure referred to as remodeling of the airways. Remodeling in asthma is characterized by the following structural changes: Hypertrophy/hyperplasia of airway smooth muscle, increase in mucus glands, thickening of the reticular basement membrane, vascular dilation/angiogenesis and ECM deposition. Mechanisms of airway remodeling involve growth factor expression, protease/antiprotease balance, chronic antigen challenge, Th2 cytokines, myofibroblast hyperplasia, leukotrienes, IL-6 group cytokines, tryptases and possible genetic susceptibility. Despite the evidence that supports a close relationship between remodeling and clinical severity, the presence of airway remodeling is considered as an independent factor in the whole pathophysiological process of the disease. Low postbronchodilator FEV1/VC ratio in early life confirms the start of airway remodeling in childhood. The efficacy of anti-inflammatory treatment on the natural course of remodeling is still debated. Inhaled corticosteroids seemed to be the ideal treatment although they suppress part of the whole remodeling process without reversing it. Recent in vivo evidence supports the beneficial effect of long acting β2 agonists. We still need further research in order to better understand the relationship between remodeling, the natural history of the disease and the early relevant markers that might predict its appearance and its progress. Pneumon 2003, 16(2):142-152.