标题：细胞衰老在特发性肺纤维化中的作用及机制研究进展

      作者：韦建茂，高胜兰，宋泽庆，刘刚    广东医科大学湛江校区，广东 湛江 524000

      卷次： 2019年30卷5期

      【摘要】 特发性肺纤维化(IPF)是一种不明原因的慢性进行性间质性肺炎，年龄是其独立的高危因素。随着年龄增长，衰老细胞积累，已有多种证据表明细胞衰老可通过衰老相关分泌表型(SASP)、端粒功能障碍、线粒体功能障碍、DNA损伤、表观遗传学改变、炎症反应和蛋白质稳态失衡等多种机制来促进 IPF的发生发展。本文就细胞衰老在 IPF中的作用和机制进行总结概述，不仅能够加深对 IPF发病机制的认识，同时也能为 IPF的预防、诊断和治疗提供理论支撑。
      【关键词】 细胞衰老；特发性肺纤维化；衰老相关分泌表型；端粒功能障碍；DNA损伤
      【中图分类号】 R563 【文献标识码】 A 【文章编号】 1003—6350（2019）05—637—06R

ole and mechanism of cellular senescence in idiopathic pulmonary fibrosis: research progress at home andabroad.
WEI Jian-mao, GAO Sheng-lan, SONG Ze-qing, LIU Gang. Guangdong Medical University (Zhanjiang Campus),Zhanjiang 524000, Guangdong, CHINA【Abstract】 Idiopathic pulmonary fibrosis (IPF) is an unexplained chronic and progressive interstitial pneumonia.Age is an independent risk factor for IPF. With the age increases, aging cells continue to accumulate. There is a varietyof evidence that cellular senescence can promote the occurrence and development of IPF through senescence-associatedsecretory phenotype (SASP), telomere dysfunction, mitochondrial dysfunction, DNA damage, epigenetic changes, in-flammatory response, protein homeostasis imbalance, and other mechanisms. This paper summarizes the role and mecha-nism of cell senescence in IPF, which not only can deepen the understanding of the pathogenesis of IPF, but also providetheoretical support for the prevention, diagnosis and treatment of IPF.
      【Key words】 Cellular senescence; Idiopathic pulmonary fibrosis; SASP; Telomere dysfunction; DNA damage·综述·doi:10.3969/j.issn.1003-6350.2019.05.029基金项目：国家自然科学基金(编号：81570062)