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
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陈则圣,在读硕士,主要研究方向为职业卫生与环境卫生学

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R135.2

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Research progress of the mechanism for PD-1 molecule regulating pulmonary fibrosis and its research prospects in silicosis
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    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。本文拟围绕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。

    Abstract:

    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.

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历史
  • 收稿日期:2022-05-25
  • 最后修改日期:2022-05-25
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  • 在线发布日期: 2022-07-22
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