Analysis of the effects of perfluorooctane sulfonate on COPD using network toxicology and molecular docking

Area of Science:

• Environmental Health
• Toxicology
• Pulmonology

Background:

• Chronic obstructive pulmonary disease (COPD) is a major global health burden.
• Environmental pollutants, such as perfluorooctane sulfonate (PFOS), are increasingly implicated in respiratory diseases.
• Understanding the molecular mechanisms linking PFOS to COPD is crucial for developing effective interventions.

Purpose of the Study:

• To elucidate the pathogenic mechanisms of PFOS in COPD using network toxicology.
• To identify key molecular targets and pathways affected by PFOS exposure in COPD.
• To explore potential therapeutic targets for PFOS-induced respiratory disorders.

Main Methods:

• Integrated multiple biological databases to identify PFOS-related targets in COPD.
• Constructed and analyzed protein-protein interaction networks to identify key proteins.
• Performed functional enrichment analysis (including GSEA) and molecular docking studies.

Main Results:

• Identified 158 PFOS-related targets in COPD, with EGFR, ESR1, GRB2, HSP90AA1, and SRC as central proteins.
• Functional analysis revealed PFOS targets key pathways in airway inflammation, oxidative stress, and immune regulation.
• Molecular docking confirmed high-affinity binding of PFOS to core targets, suggesting dysregulation of cellular processes.

Conclusions:

• PFOS significantly contributes to COPD pathogenesis by disrupting inflammatory responses, oxidative balance, and cellular proliferation.
• Key proteins like EGFR and SRC are critical mediators of PFOS toxicity in COPD.
• These findings offer novel molecular insights and potential therapeutic targets for managing environmental pollutant-aggravated respiratory diseases.