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Papers
61,005 resultsShowing papers similar to Intersection of microplastic toxicity targets and differentially expressed genes in allergic rhinitis.
ClearProtein-protein network analysis.
This study presents a protein-protein interaction network and LASSO regression analysis identifying key molecular targets through which microplastics may act in allergic rhinitis, using STRING database clustering and Genemama functional enrichment. The analysis identified three key gene targets and constructed a microplastic-target-pathway network to elucidate potential mechanistic pathways of microplastic-associated disease.
All the original data in the study.
This dataset and analysis examines the overlap between microplastic toxicity targets and differentially expressed genes in allergic rhinitis, identifying shared molecular pathways that may link microplastic exposure to the development or worsening of allergic airway disease.
Microplastic exposure and allergic rhinitis: Network toxicology, and molecular docking insights
Researchers used network toxicology and molecular docking approaches to investigate how microplastic exposure may contribute to allergic rhinitis. The study identified key molecular mediators through which microplastics may drive respiratory inflammation pathways, and found that resveratrol could potentially modulate these pathways, offering insights into the mechanisms linking microplastic exposure to allergic respiratory conditions.
KEGG enrichment analysis.
This supplementary data presents KEGG pathway enrichment analysis results from a study examining the molecular intersection between microplastic toxicity targets and genes altered in allergic rhinitis, identifying inflammatory and immune signaling pathways as key convergence points.
Workflow of the analysis.
This workflow figure illustrates the analytical pipeline used in a network toxicology study examining the intersection of microplastic molecular targets with allergic rhinitis gene expression data, from database retrieval through enrichment analysis and network construction.
Screening of differentially expressed genes and functional enrichment analysis of crossover genes in allergic rhinitis.
This figure supplement presents bioinformatics results from a study identifying crossover genes between microplastic toxicity targets and allergic rhinitis differentially expressed genes, including volcano plots, Venn diagrams, and pathway enrichment analyses.
LASSO regression screening of key targets and their internal validation analysis.
This study used LASSO regression to identify three key gene targets through which microplastics may contribute to allergic rhinitis (AR), validated through ROC curves and single-gene GSEA analysis. The results reveal differential expression profiles and enrichment pathways for these targets, providing potential diagnostic biomarkers linking microplastic exposure to AR pathogenesis.
Microplastics in Allergic Rhinitis: Multimechanistic Drivers of Barrier Disruption and Immune Dysregulation
This review examines the multimechanistic pathways by which microplastics drive barrier disruption and immune dysregulation in allergic rhinitis, considering how physical and chemical properties of microplastic particles interact with nasal epithelial and immune function. The paper synthesizes emerging evidence on microplastics as a novel contributor to upper airway allergic disease.
The impact of polyethylene terephthalate microplastics on the pathogenesis of atherosclerosis: Focusing on network toxicology and target gene detection
Researchers used network toxicology and gene analysis to investigate how PET microplastics may influence atherosclerosis, the buildup of plaque in arteries. They identified specific genes involved in inflammation and immune cell signaling that are affected by both PET exposure and atherosclerosis development. The study suggests that microplastic exposure could worsen cardiovascular disease through shared inflammatory pathways.
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.
Integrative bioinformatics analysis reveals that microplastics promote chronic rhinosinusitis with nasal polyps through NOXO1-mediated oxidative stress and myoepithelial cell reprogramming
This bioinformatics study used transcriptomic data to investigate how microplastics may promote the development of chronic rhinosinusitis with nasal polyps (CRSwNP). The analysis identified NOXO1-mediated oxidative stress and myoepithelial cell reprogramming as potential molecular mechanisms linking MP exposure to this inflammatory condition.
Preliminary Study of Microplastic in Allergic Rhinitis
Researchers compared microplastic concentrations in the nasal cavities of patients with allergic rhinitis versus healthy individuals. They found significantly higher levels of microplastics in the noses of people with the allergic condition. This preliminary finding suggests a potential connection between microplastic exposure in the nasal passages and allergic airway conditions, though more research is needed to understand the relationship.
Effect of Microplastic Inhalation on Allergic and Nonallergic Rhinitis
Researchers analyzed nasal lavage samples from rhinitis patients and healthy controls, finding significantly higher microplastic concentrations in both allergic and nonallergic rhinitis groups compared to controls. Younger participants and those with more severe symptoms tended to have higher microplastic levels in their nasal passages. The study suggests that inhaled microplastics may play a role in nasal inflammation, though more research is needed to establish a direct cause-and-effect relationship.
Detection of microplastics in patients with allergic rhinitis
In a study of 66 patients, researchers found significantly more microplastic particles in nasal wash samples from people with allergic rhinitis compared to healthy volunteers. The microplastics found were mostly fibers and fragments small enough to deposit in nasal passages during normal breathing. This is among the first studies to link airborne microplastic exposure in the nose to an allergic condition, suggesting inhaled microplastics may contribute to nasal inflammation.
Airway exposure to microplastics: Potential mechanisms from epithelial barrier damage to the development of allergic rhinitis
This review summarized the mechanisms by which airborne microplastic exposure triggers allergic rhinitis, identifying pathways including physical and chemical disruption of the airway epithelial barrier, oxidative stress from adsorbed pollutants, and induction of Th2 immune responses and IgE class-switching. The findings support airborne MPs as a novel trigger for upper respiratory allergic disease.
Inflammatory Effects of Microplastics and Nanoplastics on Nasal Airway Epithelial Cells
Researchers found that polystyrene micro- and nanoplastics cause inflammatory cytokine responses in nasal epithelial cells even over short exposure periods. The study also observed ciliary blunting and transcriptional evidence of significant inflammation and stress responses, suggesting that the nasal airway is vulnerable to plastic particle exposure.
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
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.
Impact of Micro and Nanoplastics on Inflammatory and Antioxidant Gene Expression in the Gastrointestinal System
This study examined the effects of micro- and nanoplastics on inflammatory and antioxidant gene expression in gastrointestinal tissues. The results indicate that plastic particles trigger upregulation of inflammatory markers and oxidative stress pathways in gut cells, contributing to understanding of how dietary microplastic exposure may contribute to gastrointestinal disease.
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.
Effects of microplastics on allergic airways and potential pathogenesis: a review
This review examines how microplastics, which can enter the body through breathing, eating, and skin contact, may affect allergic airway conditions. Researchers found evidence that microplastics can damage airway lining cells, disrupt the protective barrier of the respiratory tract, and trigger heightened airway reactivity. The study suggests that chronic microplastic exposure may worsen allergic airway inflammation, though more research is needed to fully understand the mechanisms involved.
Detection of microplastics in human nasal mucosa
Microplastic particles were detected for the first time in human nasal mucosa samples, with polymer types and concentrations quantified, providing direct evidence that the upper respiratory tract is a site of microplastic deposition from inhaled air.
Adverse outcome pathway networks of microplastic ecotoxicity to aquatic organisms: A critical review
Researchers used automated text-mining combined with multi-level ecotoxicological review to construct adverse outcome pathway networks for microplastic toxicity in aquatic organisms. They mapped how microplastics cause harm from initial tissue contact through molecular disturbances to higher-level biological effects in gills, gut, liver, gonads, and brain. The study found strong evidence for early-stage toxic mechanisms but identified critical knowledge gaps in understanding downstream biological consequences.
Micro- and Nanoplastics Act as Metal Carriers with the Potential to Alter Human Gene Expression Patterns—The Inferences from Bioinformatic Online Tools
This review examined how micro- and nanoplastic particles interact with and adsorb metals such as iron, copper, and zinc, and how this metal trafficking into cells alters gene expression and cellular function. The authors highlighted emerging evidence that MNPs act as metal carriers that amplify trace element toxicity and cellular stress responses.
Network toxicology and bioinformatics analysis reveal the molecular mechanisms of polyethylene terephthalate microplastics in exacerbating diabetic nephropathy
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.