Abstract
The incidence of asthma worldwide is increasing, and the disease has a large unmet clinical need. Despite the availability of anti-inflammatory and bronchodilator medication, there is persisting morbidity and mortality. New approaches are needed to understand the role that structural changes in the airways (remodelling) play in this process. Studies of the genetic basis of asthma have identified the ADAM33 (a disintegrase and metalloproteinase 33) gene, a novel member of the ADAM family of zinc-dependent metalloproteases, as a risk factor for the development of asthma and bronchial hyperresponsiveness (BHR). The identification of ADAM33 as a major risk factor involved in the pathogenesis of BHR and airway wall remodelling provides insight into the pathogenesis of asthma and represents a novel therapeutic target.