Airway vascular reactivity and vascularisation in human chronic airway disease
Pulmonary Pharmacology and Therapeutics , Volume 22 - Issue 5 p. 417- 425
Altered bronchial vascular reactivity and remodelling including angiogenesis are documented features of asthma and other chronic inflammatory airway diseases. Expansion of the bronchial vasculature under these conditions involves both functional (vasodilation, hyperperfusion, increased microvascular permeability, oedema formation, and inflammatory cell recruitment) and structural changes (tissue and vascular remodelling) in the airways. These changes in airway vascular reactivity and vascularisation have significant pathophysiological consequences, which are manifest in the clinical symptoms of airway disease. Airway vascular reactivity is regulated by a wide variety of neurotransmitters and inflammatory mediators. Similarly, multiple growth factors are implicated in airway angiogenesis, with vascular endothelial growth factor amongst the most important. Increasing attention is focused on the complex interplay between angiogenic growth factors, airway smooth muscle and the various collagen-derived fragments that exhibit anti-angiogenic properties. The balance of these dynamic influences in airway neovascularisation processes and their therapeutic implications is just beginning to be elucidated. In this review article, we provide an account of recent developments in the areas of vascular reactivity and airway angiogenesis in chronic airway diseases.
|Airway vasculature, Angiogenesis, Asthma, Bronchial circulation, Chronic obstructive airway disease, Extracellular matrix, Lymphangioleiomyomatosis, Smooth muscle, Vascular reactivity|
|Pulmonary Pharmacology and Therapeutics|
|Organisation||Erasmus MC: University Medical Center Rotterdam|
Bailey, S.R, Boustany, S, Burgess, J.K, Hirst, S.J, Sharma, H.S, Simcock, D.E, … Weckmann, M. (2009). Airway vascular reactivity and vascularisation in human chronic airway disease. Pulmonary Pharmacology and Therapeutics, 22(5), 417–425. doi:10.1016/j.pupt.2009.04.007