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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.
Childhood obesity is a severe global epidemic, and emerging evidence suggests environmental pollutants like polystyrene microplastics (PS-MPs) may disrupt metabolic homoeostasis though mechanistic insights remain limited. This study integrated cross-species transcriptomics (from zebrafish and human adipose datasets), network toxicology, machine learning, and molecular docking to explore this link. We identified 40 overlapping genes between childhood obesity related DEGs and PS-MPs related genes, enriched in lipid metabolic pathways such as cholesterol homoeostasis and insulin signalling. Topological and machine-learning analyses highlighted hub genes, which showed strong diagnostic accuracy. Molecular docking further revealed stable binding (energy < −5.0 kcal/mol) between PS-MPs and key targets (APOB、BUB1、CDC20 and PPARGC1A). Our integrative analysis suggests that PS-MPs may act as an environmental trigger that could disrupt conserved lipid and metabolic homoeostasis by targeting key hub genes (APOB、BUB1、CDC20 and PPARGC1A). These findings provide a novel molecular hypothesis linking PS-MPs exposure to childhood obesity and support precautionary measures.
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Integrative network toxicology and molecular docking preliminarily explore the potential role of polystyrene microplastics in childhood obesity
AI summary Read the abstract
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.
Integrative network toxicology and molecular docking preliminarily explore the potential role of polystyrene microplastics in childhood obesity
AI summary Read the abstract
This study found that tiny plastic particles called polystyrene microplastics (found in food packaging and disposable cups) may contribute to childhood obesity by disrupting how the body processes fats and controls metabolism. The researchers discovered that these plastic particles can bind to and interfere with key genes responsible for managing cholesterol and insulin in the body. While more research is needed, these findings suggest parents should try to limit their children's exposure to disposable plastic food containers as a precaution against obesity risk.
The toxicological impact of PET-MPs exposure on atherosclerosis: insights from network toxicology, molecular docking, and machine learning
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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.
Assessing the toxicological effects of exposure to environmental pollutants PET-MPs on vascular diseases: insights from network toxicology, molecular docking, molecular dynamics, and experimental validation
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Researchers used network toxicology, molecular docking, and cell experiments to investigate how PET microplastics may contribute to vascular diseases. They identified four core molecular targets and found that PET microplastics induced mitochondrial oxidative stress, increased reactive oxygen species, and promoted vascular smooth muscle cell death. The study provides initial molecular-level evidence that microplastic exposure may be a contributing factor in vascular damage and remodeling.
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