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Updated: Aug 6, 2026
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Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro
Published on: January 31, 2022
Identification of Core Pathways in Perfluorooctane Sulfonamide-Induced Liver Injury Using a Network Toxicology
Yan Yang1, Ye Yuan1, Renzhong Ding1
1Department of Cardiovascular Surgery, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Environmental Toxicology and Chemistry
|July 24, 2026
Summary
Perfluorooctane sulfonamide (PFOSA) exposure is linked to liver injury markers in humans. This study reveals PFOSA
Area of Science:
- Environmental Health
- Toxicology
- Bioinformatics
Background:
- Perfluorooctane sulfonamide (PFOSA) is an persistent environmental contaminant with unclear hepatotoxicity mechanisms.
- Understanding PFOSA's impact on liver health is crucial for public health and environmental regulation.
Purpose of the Study:
- To systematically explore the hepatotoxicity mechanism of PFOSA using integrated epidemiological, network toxicology, bioinformatics, and molecular docking approaches.
- To identify key molecular targets and pathways involved in PFOSA-induced liver injury.
Main Methods:
- Analysis of National Health and Nutrition Examination Survey (NHANES) data (n=2,476) to correlate PFOSA exposure with liver function markers.
- Network toxicology and bioinformatics analyses to screen PFOSA targets, construct protein-protein interaction networks, and identify core targets.
- Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, and molecular docking simulations.
- External validation using Gene Expression Omnibus (GEO) datasets.
Main Results:
- Significant association found between PFOSA exposure and elevated liver function markers (AST, ALP, TBIL) in the NHANES cohort.
- Identification of 623 intersection targets, with 37 core targets including MDM2, HSP90AB1, HIF1A, MMP9, and TP53.
- Enrichment analysis revealed pathways related to cancer, oxidative phosphorylation, and non-alcoholic fatty liver disease (NAFLD).
- Molecular docking confirmed strong binding affinity between PFOSA and identified core targets.
Conclusions:
- PFOSA may induce liver steatosis, fibrosis, and cancer risk by disrupting apoptosis (MDM2-TP53), oxidative stress (HIF1A), and extracellular matrix degradation (MMP9).
- Findings highlight the need for stricter PFOSA regulations and environmental monitoring, especially in NAFLD-prevalent areas.
- This study provides a multi-level framework for assessing PFOSA toxicity and developing intervention strategies.
