PD-1分子调控肺纤维化的机制进展及其在矽肺病研究中的展望  

Research progress of the mechanism for PD-1 molecule regulating pulmonary fibrosis and its research prospects in silicosis

作　　者：陈则圣 吴一鸣 周婷[3] 彭哲[2] 史廷明[2] 崔秀青 CHEN Ze-sheng;WU Yi-ming;ZHOU Ting;PENG Zhe;SHI Ting-ming;CUI Xiu-qing(School of Public Health,Wuhan University,Wuhan,Hubei 430071,China;Hubei Provincial Center for Disease Control and Prevention,Wuhan,Hubei 430079,China;Hubei Province Key Laboratory of Occupational Hazard Identification and Control,Wuhan University of Science and Technology,Wuhan,Hubei 430065,China)

机构地区：[1]武汉大学公共卫生学院,湖北武汉430071 [2]湖北省疾病预防控制中心,湖北武汉430079 [3]武汉科技大学职业危害识别与控制湖北省重点实验室,湖北武汉430065

出　　处：《公共卫生与预防医学》2022年第4期118-123,共6页Journal of Public Health and Preventive Medicine

基　　金：国家自然科学基金项目(81903292);职业危害识别与控制湖北省重点实验室开放基金项目(OHIC2021G07)。

摘　　要：程序性死亡因子-1(PD-1)是近年临床肿瘤免疫治疗的明星靶向分子。最新研究提示,PD-1分子及相关信号通路(PI3K/AKT、JAK/STAT3、p38MAPK、ERK等)在肺纤维化进程中也具有关键调控作用。矽肺是一种由于吸入游离二氧化硅粉尘引起的、以肺部广泛结节性纤维化为主的全身性疾病,严重危害患者的健康。分析PD-1分子在矽肺进展中的机制,可能在矽肺的机制研究和临床诊疗方面具有重要意义。拟围绕PD-1分子调控相关信号通路影响肺纤维化过程的机制研究进行综述,并对以上机制在矽肺病研究中的应用作出展望。Programmed death factor-1(PD-1)is a promising target molecule for clinical tumor immunotherapy in recent years.Recent studies suggest that PD-1 and related signaling pathways(PI3K/AKT,JAK/STAT3,p38MAPK,ERK,etc.)played a key regulatory role in the process of pulmonary fibrosis.Silicosis is a systemic disease caused by inhalation of free silicon dioxide dust,which is mainly characterized by extensive pulmonary nodular fibrosis and seriously endangers the health of patients.Dissecting the role of PD-1 in the pathogenesis of silicosis may be of great significance in the mechanism research and clinical diagnosis and treatment of silicosis.This paper reviews the regulation of PD-1 molecule on related signaling pathways and its role in pulmonary fibrosis,and looks forward to the potential application of these mechanistic studies in silicosis research.

关 键 词：程序性死亡因子-1 肺纤维化 矽肺 PI3K/AKT JAK/STAT3 P38MAPK ERK 

分 类 号：R135.2[医药卫生—劳动卫生]