SIRT1在特发性肺纤维化发病机制中的研究进展  

Research Progress of SIRT1 in Pathogenesis of Idiopathic Pulmonary Fibrosis

作　　者：何远芬 谢婷婷 闵香玉 杨信容 赵勇 HE Yuanfen;XIE Tingting;MIN Xiangyu;YANG Xinrong;ZHAO Yong(Department of Respiratory and Critical Care Medicine,Affiliated Hospital of Zunyi Medical University,Zunyi 563000,China)

机构地区：[1]遵义医科大学附属医院呼吸与危重症科,贵州遵义563000

出　　处：《医学综述》2021年第17期3371-3375,共5页Medical Recapitulate

基　　金：遵义市红花岗区科学技术项目(遵红科合社字[2017]18号)。

摘　　要：特发性肺纤维化(IPF)是一种进展性的终末期肺间质疾病,以弥漫性肺泡炎、肺泡结构紊乱和肺间质纤维化为特点。其临床特征是肺功能进行性下降,最终进展为呼吸衰竭。IPF的发生发展可能与沉默信息调节因子1(SIRT1)抑制转化生长因子-β激活的肺泡上皮细胞损伤和异常修复有关,但具体发病机制尚不清楚。SIRT1是依赖于烟酰胺腺苷二核苷酸的去乙酰化酶,可能通过抑制炎症反应、纤维化和细胞衰老及激活自噬在IPF中发挥保护作用。未来,SIRT1有望成为治疗IPF的靶向分子。Idiopathic pulmonary fibrosis(IPF) is an end-stage pulmonary interstitial disease characterized by diffuse alveolitis, alveolar structural disorders and pulmonary interstitial fibrosis.The clinical features are progressive decline in lung function and finally into respiratory failure.The occurrence and development of IPF may be related to silent information regulator 1(SIRT1) inhibiting the damage and abnormal repair of alveolar epithelial cells activated by transforming growth factor-β,although the specific pathogenesis is not yet clear.SIRT1 is a nicotinamide adenosine dinucleotide dependent deacetylase, which may play a protective role in IPF by inhibiting inflammation, fibrosis, cell senescence and activating autophagy.In the future, SIRT1 is expected to become a targeted molecule for the treatment of IPF.

关 键 词：特发性肺纤维化 沉默信息调节因子1 转化生长因子-Β 

分 类 号：R563.9[医药卫生—呼吸系统]