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HMGB1 mediates epithelial-mesenchymal transition and fibrosis in silicosis via RAGE/β-catenin signaling.

Chem Biol Interact

January 2025

Hebei Key Laboratory of Organ Fibrosis, School of Public Health, North China University of Science and Technology, Tangshan, Hebei, 063210, China. Electronic address:

Epithelial-mesenchymal transition (EMT) is implicated in the pathogenesis of silicosis. High mobility group box 1 (HMGB1) has been found to induce EMT in fibrotic diseases. Previous studies have revealed a critical role of HMGB1 in silicosis, whereas the detail mechanisms still obscure.

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Inhalation of crystalline silica particles causes silicosis, which is a severe inflammatory lung disease that is associated with granulomatous and fibrotic responses. We investigated whether silica-induced silicosis might promote airway hyperreactivity (AHR) and the role of TNF-α and thalidomide in this process. Mice received an intranasal instillation of silica particles (1.

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Silicosis, a fibrotic lung disease caused by crystalline silica inhalation, presents unique challenges in lung transplantation. This case reports an unprecedented complication in a lung transplant recipient with chronic silicosis. A man in his 60 s, post left single-lung transplantation for silica-induced pneumoconiosis, developed acute respiratory deterioration following routine bronchoscopy.

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Objective: To predict the targets of Bufei Huoxue capsule (, BFHX) using network pharmacology analysis and to explore its effects and functional targets in a silicotic rat model.

Methods: The drug and disease targets were correlated through network pharmacology analysis to explore the targets and signaling pathways of BFHX affecting silicosis. NR8383 cells were cultured to verify the core genes and pathways.

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Article Synopsis
  • Silicosis is an occupational lung disease causing lung fibrosis and poses a significant risk to workers due to a lack of effective treatments.
  • Researchers developed in vitro and in vivo models of silicosis, utilizing scRNA-sequencing to analyze lung tissue and discovered that silica nanoparticles (SiNPs) induce macrophage pyroptosis, leading to a shift in fibroblasts toward myofibroblasts.
  • The study reveals how exosomes from pyroptotic macrophages influence pro-fibrotic signaling, suggesting that SiNP exposure exacerbates lung fibrosis and highlighting potential new therapeutic targets for silicosis.
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