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Integrated computational analysis identifies FABP4, PTGS2, and HPGD as Key molecular targets linking PET microplastic exposure to metabolic dysfunction-associated steatotic liver disease
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Scientists used computer modeling to show that PET microplastics (the type found in plastic bottles and packaging) can physically bind to three proteins your liver uses to manage fat metabolism and inflammation, potentially contributing to fatty liver disease—a condition already affecting roughly a quarter to a third of people worldwide. This is an early-stage computational study, not proof that microplastics cause fatty liver disease in real life, but it gives researchers specific targets to investigate further and adds to growing concerns about how these tiny plastic particles might affect our organs.
BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) affects 25-38% of the global population, yet the contribution of environmental polyethylene terephthalate (PET) microplastics to its pathogenesis remains unclear. PET microplastics accumulate in the liver at approximately 4.6 particles per gram of tissue and have been implicated in metabolic disturbance, oxidative stress, and inflammation, but their molecular targets and mechanisms in MASLD are not well defined. METHODS: We integrated three GEO microarray cohorts (GSE37031, GSE63067, GSE89632) and performed differential expression analysis, weighted gene co-expression network analysis (WGCNA), and PET target prediction using ChEMBL, PharmMapper, and SwissTargetPrediction. Functional enrichment, protein-protein interaction network analysis, CIBERSORT-based immune deconvolution, molecular docking, and 100 ns molecular dynamics simulations were employed to identify and validate hub genes. RESULTS: Integration of MASLD transcriptomes and PET target predictions yielded 19 overlapping genes enriched in pathways related to lipid metabolism, fatty acid degradation, glycolysis/gluconeogenesis, and chemical carcinogenesis. Network topology consistently highlighted FABP4, PTGS2, and HPGD as central hub genes. Immune deconvolution revealed MASLD-associated alterations characterized by increased M2 macrophages and γδ T cells, with decreased monocytes, dendritic cells, and naive B cells. PTGS2 and FABP4 expression showed strong correlations with innate immune cells. Molecular docking demonstrated favorable PET binding to all three proteins (-6.3 to -6.9 kcal/mol), and molecular dynamics simulations confirmed stable complexes over 100 ns, with predominantly hydrophobic interactions. CONCLUSIONS: Through integrated bioinformatics analysis and molecular simulation, this study identifies FABP4, PTGS2, and HPGD as potential molecular targets through which PET microplastics may influence lipid metabolism, prostaglandin signaling, and innate immune responses in MASLD. Molecular docking and dynamics simulations suggest favorable binding interactions between PET and these proteins.
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Environmental PET-microplastic exposure and risk of non-alcoholic fatty liver disease: An integrated computational toxicology and multi-omics study
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Researchers used computational toxicology and machine learning to identify six key genes linking PET microplastic exposure to non-alcoholic fatty liver disease (NAFLD), with the model achieving high diagnostic accuracy and molecular docking suggesting that PET-derived chemicals may directly bind to proteins controlling liver fat metabolism.
Chronic PET‐Microplastic Exposure: Disruption of Gut–Liver Homeostasis and Risk of Hepatic Steatosis
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Researchers exposed mice to PET microplastics ground from plastic bottles over 29 weeks and found that the particles caused obesity, liver enlargement, fatty liver disease, and early-stage scarring of liver tissue. The microplastics also disrupted gut bacteria and bile acid metabolism, pointing to damage along the gut-liver connection. The findings raise concerns about the long-term health effects of chronic exposure to the type of microplastics commonly found in food and beverages.
Letter to the Editor: Microplastics as promoters of metabolic dysfunction-associated steatotic liver disease: Mechanistic insights and implications
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Tiny plastic particles found in our bodies—including the liver—may worsen fatty liver disease by disrupting how liver cells manage fat, handle stress, and clean out damaged parts, according to this commentary on existing lab and animal research. Since fatty liver disease is already the most common chronic liver condition worldwide and can lead to liver cancer, these findings raise concerns about how everyday plastic exposure might be affecting our health, though more human studies are needed to confirm the connection.
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Scientists grew tiny lab-made liver models and exposed them to common plastic particles (from water bottles, packaging, and other everyday plastics) for three weeks to see what happens when liver cells are around microplastics long-term. The plastics didn't kill the liver cells outright, but they did change how the cells produce and use energy, a subtler effect that could add up over time. This matters because it gives researchers a better tool to study how different types of plastic might quietly affect liver health, even without causing obvious damage.
Microplastics and nanoplastics: Emerging drivers of hepatic pathogenesis and metabolic dysfunction
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This review examines emerging evidence linking micro- and nanoplastic exposure to liver disease, including metabolic dysfunction-associated liver disease, cirrhosis, and liver cancer. Researchers found that these particles may contribute to liver damage through oxidative stress, inflammation, and disruption of metabolic pathways. The study highlights the need for further research into how environmental plastic contamination may be influencing the rising rates of liver disease worldwide.
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