Siddiqui Sana, Martin James G
Meakins Christie Laboratories, McGill University, 3626 St. Urbain Street, Montreal, Quebec H2X 2P2, Canada.
Curr Allergy Asthma Rep. 2008 Nov;8(6):540-7. doi: 10.1007/s11882-008-0098-3.
Airway remodeling in asthma is a complex process that involves structural changes in virtually all tissues of the airway wall. The histologic changes to the airways consist of epithelial proliferation and goblet cell differentiation, subepithelial fibrosis, airway smooth muscle (ASM) growth, angiogenesis, matrix protein deposition, gland hyperplasia and hypertrophy, and nerve proliferation. Cytokines, chemokines, and growth factors from inflammatory cells and structural cells contribute to remodeling. There are complex interactions among the various signaling pathways involving matrix metalloproteinases that are required for growth factor release. The physiologic consequences of remodeling are airway hyperresponsiveness from ASM growth and mucus hypersecretion from gland and goblet cell hyperplasia. Airway stiffening is a probable contributor to airway hyperresponsiveness through attenuation of the transmission of potently bronchodilating cyclical stress to the ASM during breathing. The epidermal growth factor receptor's role in remodeling and its interaction with other potential causes of remodeling are discussed.
哮喘中的气道重塑是一个复杂的过程，涉及气道壁几乎所有组织的结构变化。气道的组织学变化包括上皮细胞增殖和杯状细胞分化、上皮下纤维化、气道平滑肌（ASM）生长、血管生成、基质蛋白沉积、腺体增生和肥大以及神经增殖。炎症细胞和结构细胞产生的细胞因子、趋化因子和生长因子促成了重塑。涉及基质金属蛋白酶的各种信号通路之间存在复杂的相互作用，而基质金属蛋白酶是生长因子释放所必需的。重塑的生理后果是ASM生长导致气道高反应性，以及腺体和杯状细胞增生导致黏液分泌过多。气道僵硬可能通过在呼吸过程中减弱强效支气管扩张性周期性应力向ASM的传递而导致气道高反应性。本文讨论了表皮生长因子受体在重塑中的作用及其与其他潜在重塑原因的相互作用。
