Claudin-18对早产儿支气管肺发育不良作用的研究进展

A review on the effect of Claudin-18 on bronchopulmonary dysplasia in preterm infants

摘要:

支气管肺发育不良（bronchopulmonary dysplasia，BPD）早期以肺水肿为主要表现，晚期出现特征性的肺泡化受阻和微血管发育不良，可能由肺上皮屏障的结构和功能破坏引起。Claudin蛋白是紧密连接的主要成分，参与调节细胞旁离子和溶质渗透性。Claudin-18是目前唯一已知的肺特异性紧密连接蛋白，其缺乏可导致肺部屏障功能障碍和肺泡发育受损，其敲除可出现BPD的特征性组织学病理变化。该文将从肺上皮通透性、肺泡发育及肺部祖细胞稳态3个方面阐释Claudin-18在BPD发生发展中扮演的重要角色，旨在对BPD的发病机制研究和临床治疗提供新思路。

Abstract:

Bronchopulmonary dysplasia (BPD) has the main manifestations of pulmonary edema in the early stage and characteristic alveolar obstruction and microvascular dysplasia in the late stage, which may be caused by structural and functional destruction of the lung epithelial barrier. The Claudin family is the main component of tight junction and plays an important role in regulating the permeability of paracellular ions and solutes. Claudin-18 is the only known tight junction protein solely expressed in the lung. The lack of Claudin-18 can lead to barrier dysfunction and impaired alveolar development, and the knockout of Claudin-18 can cause characteristic histopathological changes of BPD. This article elaborates on the important role of Claudin-18 in the development and progression of BPD from the aspects of lung epithelial permeability, alveolar development, and progenitor cell homeostasis, so as to provide new ideas for the pathogenesis and clinical treatment of BPD.