Review on role of NLRP3 inflammasome in pathogenesis of silicosis

Zhenzhen Fan; Yehong Zhao; Bing LI; Yang Liu; Junyu Jiang; Min MU; Xinrong Tao

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Review on role of NLRP3 inflammasome in pathogenesis of silicosis

VernacularTitle:NLRP3炎症小体在矽肺发病机制中的作用研究概况
Author: Zhenzhen FAN ¹ ; Yehong ZHAO ¹ ; Bing LI ¹ ; Yang LIU ¹ ; Junyu JIANG ¹ ; Min MU ¹ ; Xinrong TAO ¹
Author Information

1. School of Medicine/Key Laboratory of Industrial Dust Control and Occupational Health of the Ministry of Education/Anhui Province Engineering Laboratory of Occupational Health and Safety, Anhui University of Science and Technology, Huainan, Anhui 232001, China.
Publication Type:Review
Keywords: NLRP3 inflammasome; silicosis; pulmonary fibrosis; therapy
From: Journal of Environmental and Occupational Medicine 2022;39(8):931-936
CountryChina
Language:Chinese
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.