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Polyethylene terephthalate microplastics exposure enhances the risk of ulcerative colitis: insights from multiomics integration, machine learning, and molecular docking reveal intestinal toxicity mechanisms
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Using multiomics integration, machine learning, and molecular docking, this study identified mechanisms by which PET microplastic exposure may increase the risk of ulcerative colitis. Key pathways included intestinal barrier disruption, immune dysregulation, and oxidative stress triggered by PET-MP-protein interactions.
This study offers valuable insights into the molecular mechanisms by which PET-MPs may induce UC, providing a theoretical foundation for understanding the potential health risks associated with PET-MPs exposure.
More Papers Like This
Polyethylene Terephthalate Microplastics Exposure Enhances the Risk of Ulcerative Colitis: Insights From Multi-Omics Integration, Machine Learning, and Molecular Docking Reveal Intestinal Toxicity Mechanisms: A Commentary
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This commentary discusses a study linking polyethylene terephthalate (PET) microplastics to increased risk of ulcerative colitis, using machine learning, genomic analysis, and molecular docking. The authors raise methodological questions to help strengthen this emerging line of research connecting plastic exposure to gut inflammation.
Commentary on “Polyethylene terephthalate microplastics exposure enhances the risk of ulcerative colitis: insights from multiomics integration, machine learning, and molecular docking reveal intestinal toxicity mechanisms”
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This commentary on a published study linking PET microplastic exposure to ulcerative colitis calls for methodological refinements — including the addition of a standalone PET-MP exposure group, multi-dose gradient experiments, and longer observation periods — to more rigorously establish causality, dose-response relationships, and the chronic disease dynamics relevant to real-world human microplastic exposure.
Exploring the prognostic implications of PET microplastic degradation products in colorectal cancer: insights from an integrated computational analysis on glucocorticoid pathway–mediated mechanisms
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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.
Exploring the prognostic implications of PET microplastic degradation products in colorectal cancer: insights from an integrated computational analysis on glucocorticoid pathway–mediated mechanisms
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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.
Investigation of the molecular network underlying PET-MPs-induced inflammatory bowel disease via integrated machine learning and molecular docking approaches
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Scientists used computer models to explore whether PET microplastics—tiny plastic particles from common plastic bottles and packaging—could play a role in inflammatory bowel disease (IBD), a painful digestive condition. Using data analysis and computer simulations (not tests in humans or animals), they found that a PET-related compound may bind to 14 specific genes linked to Crohn's disease and ulcerative colitis, suggesting a possible way microplastics could contribute to gut inflammation. This is early, computer-based research meant to guide future lab studies—it doesn't prove microplastics cause IBD in people, but it str
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