ArticleiScience2025
Analysis of the effects of perfluorooctane sulfonate on COPD using network toxicology and molecular docking.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Network toxicology deciphers micro- and nanoplastics-mediated mixture hazard, predictive risk assessment, and regulatory translation.Archives of toxicology · 2026Review
- Mechanistic insights into PFAS derivatives-induced coronary heart disease and atherosclerotic renal artery stenosis via integrated network toxicology and molecular modeling.Toxicology research · 2026Article
- The effects of nicotine exposure on depression: An integrative analysis combining network toxicology, molecular docking, and Mendelian randomization.Tobacco induced diseases · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study elucidates the pathogenic mechanisms of perfluorooctane sulfonate (PFOS) in chronic obstructive pulmonary disease (COPD) through network toxicology and molecular docking. By integrating multiple databases, we identified 158 PFOS-related targets in COPD, with five key proteins (epidermal growth factor receptor [EGFR], ESR1, GRB2, HSP90AA1, and SRC) showing central roles in protein interaction networks. Functional enrichment analysis revealed their involvement in key pathophysiological processes, including airway inflammatory responses, oxidative stress, and immune regulation, primarily through modulation of cell survival and proliferation pathways and immune and hormonal regulation pathways. Gene set enrichment analysis (GSEA) further validated these findings by confirming the significant enrichment of five key KEGG pathways identified in our analysis. Molecular docking studies confirmed high-affinity binding between PFOS and these core targets, indicating PFOS may dysregulate inflammatory responses, oxidative balance, and cellular proliferation in COPD pathogenesis. These findings provide critical molecular insights into environmental pollutant-aggravated respiratory disorders and highlight potential intervention targets for COPD management.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.