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Network toxicology and machine learning revealed the association between non-alcoholic fatty liver disease induced by polystyrene nanoplastics
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Using network toxicology and machine learning, researchers identified HSPD1 and NFE2L2 as core genes linking polystyrene nanoplastic exposure to non-alcoholic fatty liver disease, and confirmed in vitro that 100 nm polystyrene particles significantly increased lipid accumulation in liver cells. This study advances understanding of how ingested nanoplastics may disrupt hepatic lipid metabolism and contribute to fatty liver disease pathology.
This study systematically evaluated the hepatotoxic potential of common microplastic monomers using ADMETlab 3.0, identifying styrene (PubChem ID: 7501) as exhibiting significant hepatic toxicity. Comprehensive analysis of the CTD (Comparative Toxicogenomics Database) revealed a strong association between styrene exposure and NAFLD (Non-alcoholic fatty liver disease). We integrated target prediction data from CTD, STITCH and SwissTargetPrediction databases yielding 558 candidate targets, which were cross-referenced with 2018 NAFLD related genes from GeneCards and OMIM to identify 158 overlapping genes. Applying the NCBI GEO datasets GSE48452, GSE126848, GSE89632, and GSE63067, comprising 98 control samples and 113 NAFLD samples, we trained the model using LASSO regression, random forest, and SVM-RFE algorithms to identify the core genes HSPD1 and NFE2L2. These findings were validated in the GSE135251 cohort, which included 10 control cases and 206 NAFLD cases. In vitro experiments showed 100 nm polystyrene nanoparticles (PS-NPs) at 200 μg/mL for HepG2 and 100 μg/mL for AML12 cells significantly increased lipid accumulation by Oil Red O staining. Western blot revealed dose-dependent changes in lipid metabolism regulators ACC1, FASN and CPT1A. Preliminary RT-qPCR and immunofluorescence studies indicate that PS-NPs can upregulate HSPD1 and NFE2L2. These findings suggest that PS-NPs promote hepatic lipid accumulation by regulating HSPD1 and NFE2L2, offering new insights into the pathogenesis of environmentally induced NAFLD.
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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.
Exploring the Classic and Novel Pathogenetic Insights of Plastic Exposure in the Genesis and Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)
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This review examined how micro/nanoplastic (MNP) exposure contributes to the genesis and progression of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), the predominant liver disease in industrialized countries. Oral MNP exposure impacts the gut-liver axis, promotes steatosis through metabolic dysfunction and inflammation, and plastic additives like BPA act as exogenous factors that may trigger trained immunity pathways worsening MASLD.
Untargeted metabolomics and transcriptomics joint analysis of the effects of polystyrene nanoplastics on lipid metabolism in the mouse liver
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Mice exposed to polystyrene nanoplastics for 12 weeks gained weight without eating more and showed increased cholesterol levels and fat accumulation in their livers. Gene and metabolite analysis revealed that the nanoplastics disrupted fat metabolism pathways in the liver, essentially reprogramming how the body processes and stores fat. These findings suggest that nanoplastic exposure could be a hidden factor contributing to obesity and fatty liver disease in humans.
Integrative network toxicology and molecular docking preliminarily explore the potential role of polystyrene microplastics in childhood obesity
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Researchers used computational methods including network toxicology, machine learning, and molecular docking to explore how polystyrene microplastics might contribute to childhood obesity. They identified 40 overlapping genes between obesity-related and microplastic-affected pathways, concentrated in lipid metabolism and insulin signaling. The study suggests that polystyrene microplastics may act as environmental triggers capable of disrupting metabolic balance by interacting with key regulatory genes.
Integrative network toxicology and molecular docking preliminarily explore the potential role of polystyrene microplastics in childhood obesity
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Researchers used an integrative computational approach combining cross-species transcriptomics, network toxicology, and molecular docking to investigate potential links between polystyrene microplastic exposure and childhood obesity. They identified shared gene targets involved in lipid metabolism and insulin signaling pathways, with molecular docking confirming stable binding between microplastic compounds and key metabolic proteins. The findings provide a preliminary molecular hypothesis suggesting microplastics could disrupt metabolic processes relevant to obesity.
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