ADAM33胞外域脱落在支气管哮喘发病机制中的作用研究进展

Research progress in the role of ADAM33 ectodomain shedding in the pathogenesis of bronchial asthma

研究表明解整合素金属蛋白酶(ADAM)33蛋白可通过胞外域脱落生成可溶性ADAM33,促进嗜酸粒细胞募集、气道平滑肌细胞增殖、气道血管再生和重塑、气道平滑肌细胞生物力学改变等,从而参与哮喘的发病过程,但具体机制仍未完全明确,本文就ADAM33胞外域脱落参与哮喘气道重塑、气道高反应性、肺功能的作用及可能机制进行重点阐述。

Studies have shown that a disintegrin and metalloproteinase(ADAM)33 protein can be shed from extracellular domain to produce soluble ADAM33 which can promote eosinophil recruitment,airway smooth muscle cell proliferation,airway vascular regeneration and remodeling,and airway smooth muscle cell biomechanical changes,resulting in the involvement in the pathogenesis of asthma.The specific mechanism is not completely clear though.In this paper,we will focus on the role and possible mechanism of ADAM33 extracellular domain shedding in airway remodeling,airway hyperresponsiveness,and lung function in asthma.