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Network toxicology and bioinformatics analysis reveal the molecular mechanisms of polyethylene terephthalate microplastics in exacerbating diabetic nephropathy
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This computational study used bioinformatics to explore how polyethylene terephthalate (PET) microplastics might worsen diabetic kidney disease. The analysis identified key genes and inflammatory pathways that are affected by both PET microplastics and kidney damage in diabetes. The findings suggest that microplastic exposure could accelerate kidney problems in people who already have diabetes, though lab and clinical studies are needed to confirm this.
The escalating prevalence of diabetic nephropathy (DN) has raised concerns about environmental pollutants, particularly polyethylene terephthalate microplastics (PET-MP), as potential contributors to metabolic diseases. However, the molecular mechanisms linking PET-MP exposure to DN remain unclear. This study integrates network toxicology and bioinformatics to explore PET-MP-induced nephrotoxicity in DN. PET-MP-related toxicity targets were identified using SwissTargetPrediction and SuperPred. DN-associated differentially expressed genes (DEGs) were derived from the GSE96804 dataset. Overlapping genes were analyzed via enrichment analyses (GO, KEGG), Gene Set Variation Analysis (GSVA), and protein-protein interaction (PPI) networks. Immune cell infiltration was assessed with CIBERSORT. Key genes were identified using machine learning models (LASSO, RF, SVM-RFE) and validated by a nomogram and molecular docking. Among 10,124 DN-related DEGs, 64 overlapped with PET-MP targets. These genes were enriched in pathways like VEGF signaling, PI3K activity, and oxidative stress responses. GSVA revealed significant dysregulation in 2,258 pathways, including inflammation, immune response, and ROS metabolism. Immune infiltration analysis showed reduced CD8 + T cells, monocytes, and neutrophils in DN, alongside increased Tregs and M2 macrophages. Machine learning models identified CASP3 and GRB2 as key feature genes, validated by robust cross-validation and two independent DN datasets. Molecular docking indicated favorable binding affinities of PET to CASP3 (Vina score: -5.3) and GRB2 (Vina score: -5.2), suggesting disruptions in apoptosis and signal transduction pathways. PET-MP may exacerbate DN by disrupting critical molecular and cellular pathways, compromising the regulation of apoptosis, immune responses, and cellular homeostasis. CASP3 and GRB2 emerge as central mediators, providing mechanistic insights into PET-MP-driven nephrotoxicity. This study underscores the role of environmental microplastics in metabolic disorders and highlights potential therapeutic targets for DN.
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Toxicological Effects of Polyethylene Terephthalate Microplastics on Chronic Kidney Disease: An Integrative Bioinformatics, Network Toxicology, and Machine Learning Study.
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This study used computer-based methods, including gene databases and molecular docking, to examine how PET plastic particles might affect chronic kidney disease. The analysis identified seven genes that both PET microplastics and kidney disease may affect, often related to immune, inflammation, and energy processes. No animals or human volunteers were tested directly.
Network Toxicology and Multi-omics Analysis
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This is a duplicate entry for data and code supporting a computational study on how microplastics may contribute to diabetic kidney disease. The parent study used network analysis and molecular modeling to identify potential biological mechanisms linking microplastic exposure to kidney damage.
Network Toxicology and Multi-omics Analysis
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This entry contains data and code supporting a study that used computational methods to investigate how microplastics may worsen diabetic kidney disease at the molecular level. The parent study suggests microplastics could affect kidney health through specific biological pathways, though this entry itself is a data repository rather than a full paper.
Unveiling the molecular toxicity of plasticizers derived from microplastics (DMP and DEP) in diabetic kidney disease: integrative insights from network toxicology and multi-omics analysis
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Scientists found that two chemicals commonly released from microplastics (used to make plastics flexible) can damage kidney cells in lab tests, and this damage got worse when combined with high blood sugar levels similar to those seen in diabetes. This early-stage research points to specific genes that may explain how these plastic chemicals harm kidney health, but the findings come from cell studies, not humans, so more research is needed before we know if this applies to real-world diabetic kidney disease. Still, it raises important questions about whether everyday plastic exposure could compound health risks for people with diabetes.
Computational prediction of potential aggravating mechanisms of polyethylene terephthalate microplastics in diabetic foot ulcers: An integrated in silico approach combining network toxicology, bioinformatics, machine learning, and molecular dynamics simulations
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Using computer modeling (not actual patient testing), researchers found clues that tiny plastic particles from PET plastic (commonly used in water bottles and food packaging) might make diabetic foot ulcers worse by interfering with genes that help repair cell damage and regulate blood sugar processing. While these findings are just a starting point—based on computer simulations rather than lab or human studies—they add to growing concerns that microplastics in our environment could impact chronic health conditions like diabetes complications, making this an area worth watching as research continues.
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