樊珍珍, 赵叶红, 李兵, 刘洋, 蒋峻宇, 穆敏, 陶欣荣. NLRP3炎症小体在矽肺发病机制中的作用研究概况[J]. 环境与职业医学, 2022, 39(8): 931-936. DOI: 10.11836/JEOM21541
引用本文: 樊珍珍, 赵叶红, 李兵, 刘洋, 蒋峻宇, 穆敏, 陶欣荣. NLRP3炎症小体在矽肺发病机制中的作用研究概况[J]. 环境与职业医学, 2022, 39(8): 931-936. DOI: 10.11836/JEOM21541
FAN Zhenzhen, ZHAO Yehong, LI Bing, LIU Yang, JIANG Junyu, MU Min, TAO Xinrong. Review on role of NLRP3 inflammasome in pathogenesis of silicosis[J]. Journal of Environmental and Occupational Medicine, 2022, 39(8): 931-936. DOI: 10.11836/JEOM21541
Citation: FAN Zhenzhen, ZHAO Yehong, LI Bing, LIU Yang, JIANG Junyu, MU Min, TAO Xinrong. Review on role of NLRP3 inflammasome in pathogenesis of silicosis[J]. Journal of Environmental and Occupational Medicine, 2022, 39(8): 931-936. DOI: 10.11836/JEOM21541

NLRP3炎症小体在矽肺发病机制中的作用研究概况

Review on role of NLRP3 inflammasome in pathogenesis of silicosis

  • 摘要:

    矽肺是全世界最常见的尘肺病类型之一,从事采矿、建筑和陶瓷等诸多行业的工人有较高的发病风险。职业工人长期反复吸入5 μm以下的游离二氧化硅(SiO2)粉尘引起炎症反应,进而形成以双肺广泛结节性纤维化为特征的间质性肺疾病。即使工人调离矽尘作业环境,矽肺仍在进行性发展。矽肺的发病机制复杂,Nod样受体家族蛋白3(NLRP3)炎症小体在矽肺发病与进展中的作用有待深入研究。NLRP3炎症小体是一种由NLRP3、凋亡相关斑点样蛋白和半胱天冬酶-1组成的多蛋白复合物,参与氧化应激、炎症反应、细胞凋亡和细胞焦亡四个途径,是矽肺的研究热点之一。本文首先概述了NLRP3炎症小体的结构、功能和激活机制;进而分析了NLRP3炎症小体参与矽肺发生与进展的细胞和分子机制,包括氧化应激、炎症反应、细胞凋亡和细胞焦亡;最后总结了基于不同机制的矽肺治疗药物。本文提出未来应多关注NLRP3炎症小体在矽肺发生发展中的作用,以期为矽肺的防治提供新的思路。

     

    Abstract:

    Silicosis is one of the most common forms of pneumoconiosis globally. Workers who engage in mining, construction, ceramics, and many other industries have a high risk of developing silicosis. Chronic and repeated inhalation of free silica (SiO2) dust (<5 μm) during working can lead to inflammatory reactions, resulting in interstitial lung disease characterized by extensive nodular fibrosis in both lungs. Once silicosis occurs, it will develop progressively even when the workers are removed from the silica dust environment. The pathogenesis of silicosis is complex, especially the role of nod-like receptor family protein 3 (NLRP3) inflammasome in the pathogenesis and progression of silicosis remains to be further studied. NLRP3 inflammasome, a multi-protein complex composed of NLRP3, apoptosis-associated speck-like protein, and cysteinyl aspartate specific proteinase 1 is involved in oxidative stress, inflammatory response, apoptosis, and pyroptosis, and has become one of the hot spots in silicosis research. This review summarized the structure, function, and activation mechanism of NLRP3 inflammasome. Furthermore, the cellular and molecular mechanisms of NLRP3 in mediating oxidative stress, inflammatory response, apoptosis, and pyroptosis in the progression of silicosis were reviewed. Finally, the potential therapeutic drugs for silicosis based on NLRP3-associated mechanisms were outlined. More attention should be paid to the role of NLRP3 inflammasome in the pathogenesis and progression of silicosis in the future, which will provide new ideas for the prevention and treatment of silicosis.

     

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