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Papers
20 resultsShowing papers similar to Environmental PET-microplastic exposure and risk of non-alcoholic fatty liver disease: An integrated computational toxicology and multi-omics study
ClearThe toxicological impact of PET-MPs exposure on atherosclerosis: insights from network toxicology, molecular docking, and machine learning
Researchers used network toxicology, molecular docking, and machine learning to identify how PET microplastics may promote atherosclerosis, narrowing 28 candidate targets to seven key genes and predicting interactions with atherosclerosis-relevant pathways including inflammation and lipid metabolism.
A computational framework for multi-scale data fusion in assessing the associations between micro- and nanoplastics and human hepatotoxicity
Researchers developed a computational toxicology framework integrating multi-source data and network analysis to map associations between micro- and nanoplastics and hepatotoxicity, identifying key molecular pathways through which MNPs may damage the liver, offering a scalable alternative to traditional in vivo testing.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
This study examined how polypropylene microplastics accumulate in and damage the mouse liver, using integrated lipidomics and transcriptomics to map the molecular landscape of microplastic-induced lipid disruption and metabolic dysfunction.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Proteomic and lipidomic profiling of mouse livers after polypropylene microplastic exposure revealed crosstalk between hepatic lipid fluctuations, nutrient metabolism disorders, and energy pathway disarrangements, providing mechanistic insight into microplastic-induced liver toxicity.
Integrative network toxicology and molecular docking preliminarily explore the potential role of polystyrene microplastics in childhood obesity
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.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Mouse liver studies with polypropylene microplastics revealed interconnected disruptions in lipid metabolism, nutrient processing, and energy balance, with proteomic and transcriptomic data highlighting the complexity of hepatic responses to chronic microplastic exposure.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Researchers used combined lipidomic and transcriptomic analysis to demonstrate that polypropylene microplastics accumulated in mouse liver and disrupted key metabolic pathways including lipid biosynthesis, cholesterol metabolism, and energy homeostasis.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
This study assessed the liver toxicity of polypropylene microplastics in mice using combined lipidomics and transcriptomics, identifying disrupted lipid metabolism, altered cholesterol handling, and fibrotic tissue remodeling as key pathological outcomes.
Integrative network toxicology and molecular docking preliminarily explore the potential role of polystyrene microplastics in childhood obesity
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.
Exploring the prognostic implications of PET microplastic degradation products in colorectal cancer: insights from an integrated computational analysis on glucocorticoid pathway–mediated mechanisms
Combining network toxicology, machine learning, and molecular docking, this study found that PET plastic degradation products ethylene glycol and terephthalic acid may influence colorectal cancer prognosis through 43 shared genes linked to TNF/IL-17 signaling and glucocorticoid-mediated metabolic pathways.
Molecular Landscape Remodeling Unravels the Cross-Links of Microplastics-Induced Lipidomic Fluctuations, Nutrient Disorders and Energy Disarrangements
Researchers fed mice polypropylene microplastics chronically and used lipidomics and transcriptomics to show that microplastics accumulated in the liver and disrupted lipid metabolism, cholesterol homeostasis, and redox balance, with high doses causing fibrotic liver changes.
Molecular LandscapeRemodeling Unravels the Cross-Linksof Microplastics-Induced Lipidomic Fluctuations,Nutrient Disorders and Energy Disarrangements
Researchers examined polypropylene microplastic retention in mouse liver using lipidomics and transcriptomics, finding that chronic exposure disrupted lipid metabolism, cholesterol turnover, and antioxidant defense, with high-dose treatment causing regional liver fibrosis.
Rank-In Integrated Machine Learning and Bioinformatic Analysis Identified the Key Genes in HFPO-DA (GenX) Exposure to Human, Mouse, and Rat Organisms
Researchers used integrated machine learning and bioinformatic analysis to identify key molecular markers and pathways associated with microplastic-induced biological effects, generating mechanistic hypotheses for further experimental validation.
Integrated transcriptomic and metabolomic analyses to decipher the regulatory mechanisms of polystyrene nanoplastic-induced metabolic disorders in hepatocytes
Using combined transcriptomic and metabolomic analysis, this study found that polystyrene nanoplastics disrupt lipid and amino acid metabolism in hepatocytes, identifying key regulatory genes and providing data relevant to assessing health risks from nanoplastic exposure.
Microplastics and nanoplastics: Emerging drivers of hepatic pathogenesis and metabolic dysfunction
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.
Are Ingested or Inhaled Microplastics Involved in Nonalcoholic Fatty Liver Disease?
This review explored the potential connection between microplastic exposure through ingestion and inhalation and nonalcoholic fatty liver disease, which has become a leading cause of chronic liver injury. The study discusses how dietary and environmental microplastic exposure could potentially influence liver health through mechanisms including inflammation and endocrine disruption, though further research is needed to establish definitive links.
Exploring the prognostic implications of PET microplastic degradation products in colorectal cancer: insights from an integrated computational analysis on glucocorticoid pathway–mediated mechanisms
This computational study investigated how PET microplastic degradation products affect colorectal cancer prognosis, identifying 43 genes linking ethylene glycol and terephthalic acid exposure to cancer pathogenesis via chronic inflammation mediated through TNF/IL-17 and glucocorticoid metabolic pathways.
Predicting the toxicity of microplastic particles through machine learning models
Researchers applied machine learning models to predict the toxicity of microplastic particles from their physical and chemical properties, addressing the challenge that microplastics lack the standardized identifiers used for chemical hazard classification. The models successfully predicted toxicity outcomes from particle descriptors, offering a framework for hazard screening of the diverse and complex microplastic contaminant class.
Adipose tissue as target of environmental toxicants: focus on mitochondrial dysfunction and oxidative inflammation in metabolic dysfunction-associated steatotic liver disease
This review examines how environmental toxicants, including micro and nanoplastics, target fat tissue and contribute to metabolic diseases like obesity, diabetes, and fatty liver disease. These pollutants disrupt mitochondria (the energy-producing parts of cells) and trigger a cycle of oxidative stress and inflammation that damages both fat tissue and the liver. The findings suggest that microplastic exposure could be one of several environmental factors contributing to the rising rates of metabolic disease worldwide.
Exploring the prognostic implications of PET microplastic degradation products in colorectal cancer: insights from an integrated computational analysis on glucocorticoid pathway–mediated mechanisms
Researchers used network toxicology, machine learning, and molecular docking to investigate how PET degradation products—ethylene glycol and terephthalic acid—affect colorectal cancer prognosis through the glucocorticoid signaling pathway. The analysis identified 43 shared target genes, suggesting that PET breakdown products may worsen colorectal cancer outcomes by dysregulating glucocorticoid-mediated anti-inflammatory and cell survival signals.