The vascular changes which occur in airways diseases such as asthma are starting to attract considerable attention from the respiratory research community. In addition to the vascular engorgement which occurs as part of the acute inflammatory process, several groups have demonstrated increased new vessel formation (angiogenesis) in chronic asthma.^1–,³ Not only does this occur in adult asthma, but recent studies suggest it is a prominent feature of childhood asthma, suggesting that vascular remodelling may occur relatively early in the asthmatic process.⁴ The increased airway wall thickening produced by the expanded vasculature causes enhanced airway narrowing on stimulation with constrictor agents, thereby contributing to bronchial hyper-responsiveness. Furthermore, the increased blood flow may increase inflammatory cell trafficking and exudation and transudation of cytokines and mediators and contribute to airway hyper-responsiveness by supporting the increased airway smooth muscle mass which is a key feature of asthma histopathology.⁵

There are a number of candidate angiogenic factors for these changes, perhaps the most important of which are vascular endothelial growth factor (VEGF) and angiopoietin-1, distinct molecules which act together at different stages of angiogenic processes in several biological systems.^{6,7,8,9,10,11, …}