Department of Public Health, 74496Jining Medical University, Jining, China.
Jining No. 1 People's Hospital, Jining, China.
Toxicol Ind Health. 2021 Apr;37(4):240-250. doi: 10.1177/0748233721989896. Epub 2021 Feb 16.
Silicosis is an occupational fibrotic lung disease caused by inhaling large amounts of crystalline silica dust. Transforming growth factor-β1 (TGF-β1), which is secreted from macrophages, has an important role in the development of this disease. Macrophages can recognize and capture silicon dust, undergo M2 polarization, synthesize TGF-β1 precursors, and secrete them out of the cell where they are activated. Activated TGF-β1 induces cells from different sources, transforming them into myofibroblasts through autocrine and paracrine mechanisms, ultimately causing silicosis. These processes involve complex molecular events, which are not yet fully understood. This systematic summary may further elucidate the location and development of pulmonary fibrosis in the formation of silicosis. In this review, we discussed the proposed cellular and molecular mechanisms of production, secretion, activation of TGF-β1, as well as the mechanisms through which TGF-β1 induces cells from three different sources into myofibroblasts during the pathogenesis of silicosis. This study furthers the medical understanding of the pathogenesis and theoretical basis for diagnosing silicosis, thereby promoting silicosis prevention and treatment.
矽肺是一种由吸入大量结晶二氧化硅粉尘引起的职业性纤维肺疾病。转化生长因子-β1（TGF-β1）是由巨噬细胞分泌的，在疾病的发展中起着重要作用。巨噬细胞可以识别和捕获硅尘，发生 M2 极化，合成 TGF-β1 前体，并将其从细胞内分泌出来，在细胞外被激活。激活的 TGF-β1 通过自分泌和旁分泌机制诱导来自不同来源的细胞，将其转化为肌成纤维细胞，最终导致矽肺。这些过程涉及复杂的分子事件，目前尚未完全了解。本系统综述可能进一步阐明矽肺形成过程中肺纤维化的发生和发展的部位。在这篇综述中，我们讨论了 TGF-β1 的产生、分泌和激活的拟议细胞和分子机制，以及在矽肺发病机制中 TGF-β1 如何通过三种不同来源的细胞诱导成肌成纤维细胞的机制。这项研究促进了对矽肺发病机制和诊断理论基础的医学理解，从而促进了矽肺的预防和治疗。
