Airway Pathobiology Laboratory, Department of Physiology, Monash University, Melbourne, Victoria, Australia.
Proc Am Thorac Soc. 2009 Dec;6(8):673-7. doi: 10.1513/pats.200907-064DP.
Expansion of the airway wall vascular compartment has recently been established as a feature of asthma involving both enlargement of existing vascular structures and the formation of new vessels (angiogenesis). Both processes are likely to occur together and are fundamental for supporting the many aspects of tissue inflammation and remodeling manifest in the clinical symptoms of airway disease. Multiple growth factors are implicated in airway angiogenesis, with vascular endothelial growth factor among the most important. Other asthma-associated stimuli, including ADAM33, environmental tobacco smoke, and rhinovirus infection, are emerging as proangiogenic regulators. Increasing attention is also focused on the complex interplay of airway wall inflammatory and structural cells, including airway smooth muscle in driving expansion of the bronchial submucosal vascular plexus in asthma. Here, we provide a brief update on recent developments in this emerging area and highlight the potential role played by airway smooth muscle.
气道壁血管腔的扩张最近被确定为涉及哮喘的一个特征，包括现有血管结构的扩大和新血管的形成（血管生成）。这两个过程可能同时发生，对于支持气道疾病的临床症状中表现出的组织炎症和重塑的许多方面是至关重要的。多种生长因子参与气道血管生成，其中血管内皮生长因子最重要。其他与哮喘相关的刺激物，包括 ADAM33、环境烟草烟雾和鼻病毒感染，正在成为促血管生成的调节因子。人们也越来越关注气道壁炎症和结构细胞之间的复杂相互作用，包括气道平滑肌，它们在驱动哮喘中支气管黏膜下血管丛的扩张中发挥作用。在这里，我们简要介绍这一新兴领域的最新进展，并强调气道平滑肌可能发挥的作用。
