ArticleFrontiers in medicine2025
The updated evidence of pirfenidone treated silicosis based on network pharmacology, molecular docking and experimental validation.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- 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
- Development and optimization of green extraction of naringin inRSC advances · 2025Article
- PDE4-Selective Inhibition in Chronic Obstructive Pulmonary Disease and Pulmonary Fibrosis: Different Agents or Different Targets?Life (Basel, Switzerland) · 2025Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Silicosis remains a debilitating occupational lung disease with limited therapeutic options, despite emerging evidence supporting pirfenidone's (PFD) anti-fibrotic efficacy in clinical practice. However, the molecular circuitry governing PFD's therapeutic actions in silicosis remains incompletely mapped, hindering mechanism-driven therapeutic optimization. To bridge this knowledge gap, we executed network pharmacology to replenish its molecular mechanisms and potential therapeutic targets. Materials and methods: We replicated a silicosis C57BL6/J mouse model and evaluated inflammation and fibrosis using HE, Masson, and Sirius Red staining assays. The expression of fibrotic markers Results: PFD alleviated the level of inflammation and collagen deposition and fibrotic markers Conclusion: In conclusion, we identified TNF, MMP9, NF-κB1 and TLR2, that contribute to the therapeutic effects of PFD in silicosis. Mechanistically, PFD appears to mitigate silicosis pathogenesis through suppression of epithelial TLR2/NF-κB pathway activation.
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