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Integrated network toxicology, machine learning, molecular docking and experimental validation to elucidate mechanism of polyethylene terephthalate microplastics inducing periodontitis
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Researchers combined computational biology, machine learning, and laboratory experiments to explore how polyethylene terephthalate microplastics might contribute to periodontitis, a common gum disease. They identified key molecular targets and signaling pathways through which microplastics could promote gum tissue inflammation. The study provides the first evidence linking microplastic exposure to the biological mechanisms underlying periodontal disease.
Growing evidence highlights the health risks of micro-plastics (MPs) exposure, with reported accumulations in enclosed anatomical sites such as the heart, placenta, and circulatory system. However, the role of MPs in periodontitis remains unexplored. This study employed bioinformatics, network toxicology, machine learning, molecular docking, and experimental approaches to explore the effects and underlying mechanisms of polyethylene terephthalate microplastics (PET-MPs) induced periodontitis. Multi-database screening, including GEO, ChEMBL, STITCH, GeneCards, OMIM, identified 23 candidate targets linked to PET-MPs exposure. Furthermore, we used STRING, Cytoscape software and machine learning approaches to identified 13 core targets. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment and immune cell infiltration analyses revealed that PET-MPs influence immune-related pathways, such as C-type lectin receptor signaling, VEGF receptor signaling, and TNF signaling. Molecular docking revealed high-affinity binding interactions between PET-MPs and core targets, implicating direct interference with cellular processes. Experimental assays using gingival fibroblasts (GFs) exposed to PET-MPs showed dose-dependent cytotoxicity oxidative stress induction, and pro-inflammatory activation. PET-MPs upregulated inflammation-related markers including Caspase 3, KDR, PIM2, PTGS2, MTOR, MAPK14; while downregulating AKT1 and ALPL. These findings establish a mechanistic framework linking PET-MPs exposure to periodontitis progression via redox-inflammatory crosstalk, offering novel insight into the potential pathogenesis of microplastics on periodontitis.
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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.
Micro- and nanoplastics in periodontitis: mechanistic pathways and clinical implications
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Tiny plastic particles from water, food, and even toothpaste may be doing more than just floating around your mouth, this review of existing research suggests they could worsen gum disease by fueling inflammation, disrupting the balance of oral bacteria, and interfering with how your body repairs bone and tissue. The evidence so far comes mostly from lab studies, not large human trials, so microplastics shouldn't be seen as a proven cause of gum disease, but they're a plausible piece of the puzzle worth watching, especially since periodontitis is linked to broader health issues like heart disease and diabetes.
Evaluating the toxicological effects of PET-MPs exposure on atherosclerosis through integrated network toxicology analysis and experimental validation
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Researchers used network toxicology analysis and laboratory experiments to investigate how polyethylene terephthalate microplastics may contribute to atherosclerosis. They identified several molecular targets and biological pathways through which these microplastics could promote plaque formation in blood vessels. The study provides preliminary evidence that a commonly encountered type of microplastic may interact with cardiovascular disease mechanisms, though further research is needed to confirm these findings.
Exploring the Potential Mechanism of Polyethylene Terephthalate Associated Cardiotoxicity through Network Toxicology and Molecular Docking
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Researchers used computational approaches including network toxicology, molecular docking, and molecular dynamics simulations to explore how polyethylene terephthalate microplastics may affect cardiovascular function. The study identified potential molecular pathways through which PET exposure could contribute to cardiotoxicity. The findings provide a theoretical framework for understanding how plastic contaminants might interact with heart-related biological targets.
Unveiling the pathogenic mechanisms of polyethylene terephthalate-microplastic-driven osteoarthritis and rheumatoid arthritis: PTGS2 signaling hub-oriented toxicity profiling
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Researchers used computational analysis to investigate how PET microplastics might contribute to joint diseases like osteoarthritis and rheumatoid arthritis. They identified the PTGS2 gene, involved in inflammation, as a central hub connecting microplastic exposure to joint disease pathways. The study suggests that microplastics may worsen joint inflammation through specific molecular mechanisms, though further laboratory and clinical research is needed to confirm these computational findings.
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