ArticleInternational journal of molecular sciences2022
Thalidomide Alleviates Pulmonary Fibrosis Induced by Silica in Mice by Inhibiting ER Stress and the TLR4-NF-κB Pathway.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Network meta-analysis of pharmacological treatments for idiopathic pulmonary fibrosis: evaluating effects on lung function.Frontiers in pharmacology · 2026Pooled it
- Curcumin Improves Silica Induced Lung Fibrosis by Targeting TLR4-NLRP3 Inflammasome and TGF-β Inhibition in Mice Model.Journal of biochemical and molecular toxicology · 2026Article
- Selenium nanoparticle-enhanced resveratrol suppresses pulmonary inflammation and fibrogenesis in silicosis via redox-mediated inflammatory pathway modulation.Inflammopharmacology · 2026Article
- Targeting CRBN With Thalidomide Suppresses Fibrosis After Glaucoma Drainage Surgery Through NF-κB Pathway Inhibition.Investigative ophthalmology & visual science · 2026Article
- Developments in the connection between epithelial‑mesenchymal transition and endoplasmic reticulum stress (Review).International journal of molecular medicine · 2025Review
- Zafirlukast ameliorates lipopolysaccharide and bleomycin-induced lung inflammation in mice.BMC pulmonary medicine · 2024Article
- Effect of Sex Differences in Silicotic Mice.International journal of molecular sciences · 2022Article
- Thalidomide Attenuates Skin Lesions and Inflammation in Rosacea-Like Mice Induced by Long-Term Exposure of LL-37.Drug design, development and therapy · 2022Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Silicosis is the most prevalent occupational disease in China. It is a form of pulmonary fibrosis caused by the inhalation of silicon particles. As there is no cure for the potentially lethal and progressive condition, the treatment of silicotic fibrosis is an important and difficult problem to address. Thalidomide, a drug with anti-inflammatory and immunoregulatory properties, has been reported to have lung-protective effects. The purpose of this study was to observe the therapeutic effect of thalidomide on silicotic mice and to determine the protective mechanism. By using silicotic mice models and MH-S cells, we found the expression of endoplasmic reticulum stress (ER stress) and Toll-like receptor 4 (TLR4)-nuclear factor kappa-B (NF-κB) pathway as well as inflammation-related factors were upregulated in the macrophages of silicotic mice. The same indexes were detected in silica-stimulated MH-S cells, and the results were consistent with those in vivo. That is, silica activated ER stress and the TLR4-NF-κB pathway as well as the inflammatory response in vitro. Treating both silicotic mice and silica-stimulated MH-S cells with thalidomide inhibited ER stress and the TLR4-NF-κB pathway as well as the inflammatory response. The present study demonstrates thalidomide as a potential therapeutic agent against silicosis.
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