ArticlePloS one2025
Microplastic exposure and allergic rhinitis: Network toxicology, and molecular docking insights.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
- Erratum issued
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicroplastics (MPs), ubiquitous environmental pollutants, are increasingly associated with global health risks, yet their role in allergic rhinitis (AR) pathogenesis remains poorly understood.
methodsToxicity profiles of four typical MPs (polyethylene [PE], polypropylene [PP], polyvinyl chloride [PVC], polystyrene [PS]) were evaluated using ADMETlab 3.0. MP-related targets and AR-associated genes were integrated from the CTD database and GSE43523 dataset. Functional enrichment (GO/KEGG) and PPI network analysis (STRING/GeneMANIA) were performed on overlapping genes. LASSO regression and expression validation identified key targets, and molecular docking (Autodock Vina) assessed interactions with potential therapeutics predicted by CTD.
resultsADMET analysis revealed MPs exhibit significant respiratory toxicity and ocular toxicity. We identified 301 MP toxicity targets, 1,026 AR differentially expressed genes (DEGs), and 15 overlapping pathogenic targets. Functional enrichment (GO/KEGG) demonstrated MPs disrupt respiratory mucosal homeostasis via apoptosis, mitochondrial autophagy, and inflammatory pathways. PPI network analysis and LASSO regression pinpointed DNAJB9, SQSTM1, and MAPK9 as core mediators: these genes were significantly downregulated in AR patients (P < 0.05) and displayed robust diagnostic performance (AUC = 0.82-0.93). Molecular docking revealed resveratrol binds these targets with high affinity, surpassing SQSTM1 (-5.8 kcal/mol) and MAPK9 (-6.8 kcal/mol), suggesting its potential to block MP-induced dysregulation.
conclusionsMPs drive AR pathogenesis through respiratory toxicity pathways, with DNAJB9, SQSTM1, and MAPK9 serving as critical molecular mediators. Resveratrol, by modulating target-mediated programmed cell death, emerges as a promising therapeutic candidate for mitigating MP-induced AR.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.