Download full-text PDF

Source
http://dx.doi.org/10.1016/j.arbres.2019.02.026DOI Listing

Publication Analysis

Top Keywords

silicosis sjögren's
4
sjögren's syndrome
4
silicosis
1
syndrome
1

Similar Publications

Objective: Silicosis is a pneumoconiosis characterized by fibrosis of the lung parenchyma caused by the inhalation of silica particles. Silica dust inhalation is associated with inflammation and induction of oxidative stress in the lungs. This oxidative stress affects telomeres, which are short tandem DNA repeats that cap the end of linear chromosomes.

View Article and Find Full Text PDF

Silicosis represents a formidable occupational lung pathology precipitated by the pulmonary assimilation of respirable crystalline silica particulates. This condition engenders a cascade of cellular oxidative stress via the activation of bioavailable silica, culminating in the generation of reactive oxygen species (ROS). Such oxidative mechanisms lead to irrevocable pulmonary impairment.

View Article and Find Full Text PDF

Pneumoconiosis is the occupational disease with the highest proportion in China. This study conducted a retrospective analysis of 5,791 deceased pneumoconiosis patients. In this study, males comprised 93.

View Article and Find Full Text PDF

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.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!