肺泡Ⅱ型上皮细胞在特发性肺纤维化过程中的变化  

The changes of alveolar typeⅡepithelial cells in the process of idiopathic pulmonary fibrosis

作　　者：李国杰 邓轶方 刘珉宇 LI Guojie;DENG Yifang;LIU Minyu(State Key Lab.of New Drug and Pharmaceutical Process,Shanghai Institute of Pharmaceutical Industry,China State Institute of Pharmaceutical Industry,Shanghai 200437,China;Shanghai Professional and Technical Service Center for Biological Material Drug-ability Evaluation,Shanghai 200437,China)

机构地区：[1]中国医药工业研究总院创新药物与制药工艺国家重点实验室,上海200437 [2]上海市生物物质成药性评价技术服务平台,上海200437

出　　处：《世界临床药物》2024年第11期1187-1191,共5页World Clinical Drug

基　　金：国家十三五“重大新药创制”科技重大专项项目(2019ZX09201001-004-004)。

摘　　要：肺泡Ⅱ型上皮细胞(alveolar type Ⅱ epithelial cells,AT2)作为肺泡上皮干细胞,具有很强的增殖及分化潜能,在维持肺稳态以及肺损伤修复过程中起着至关重要的作用。研究表明,当AT2正常功能遭到破坏,并演变为促纤维化表型时,就可能引起特发性肺纤维化(idiopathic pulmonary fibrosis)。作为位于黏膜表面的细胞,AT2不可避免地暴露于环境压力之下,这种压力能够产生长期影响,最终促进纤维化的发展。同时,基因突变也可能导致AT2功能受损及肺纤维化的出现。此外,衰老也是增加AT2发生病理性变化的重要因素之一。该文讨论AT2的再生过程以及造成AT2衰老、凋亡、功能障碍的信号通路。Alveolar typeⅡepithelial cells(AT2),as alveolar epithelial stem cells,possess significant proliferative and differentiation potential,plays a crucial role in maintaining lung homeostasis and the repair of lung injury.Studies have shown that idiopathic pulmonary fibrosis would occur when the normal function of AT2 is disrupted and transforms into fibrosis-promoting phenotype.Being located on the mucosal surface,AT2 is inevitably exposed to environmental stress,which can have long-lasting effects and ultimately promote the development of fibrosis.At the same time,genetic mutations may also lead to impaired AT2 function and the occurrence of pulmonary fibrosis.Additionally,aging is also one of the significant factors that increase the pathological changes in AT2.The article discussed the regeneration process of AT2 and the pathways that lead to AT2 aging,apoptosis,and dysfunction.

关 键 词：肺泡上皮细胞 肺纤维化 干细胞再生 细胞衰老 细胞凋亡 

分 类 号：R563.9[医药卫生—呼吸系统]