ArticleClinical and experimental medicine2025
Novel molecular mechanisms of eosinophil-mediated chronic obstructive pulmonary disease induced by bezo[a]pyrene.
Article in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
This study aimed to explore molecular mechanisms of benzo[a]pyrene (B[a]P) induced eosinophil-associated chronic obstructive pulmonary disease (COPD) via network toxicology and molecular dynamics modeling. Analyze chemical structures using PubChem, integrate STITCH, Swiss Target Prediction and ChEMBL databases to predict potential target molecules; use ADMETlab to assess physicochemical properties and PROTOX to predict toxicity; combine STRING and Cytoscape (based on UniProt data standardization) to screen core disease-related target molecules; conduct Gene Ontology (GO)/Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, focusing on inflammation and immune regulation pathways; perform molecular docking using AutoDock; visualize key binding sites using PyMOL/Discovery Studio; conduct 100-ns molecular dynamics simulations using Gromacs; and systematically assess the stability and dynamic mechanisms of the B[a]P-target complex based on root-mean-square deviation (RMSD) fluctuations and changes in radius of gyration. This study screened 48 potential targets related to eosinophils in COPD through protein interaction analysis, focusing on five core targets: PTPRC, SRC, AKT1, MYC, and CSF-1R. GO and KEGG analyses revealed their involvement in inflammation- and immune-related biological processes and signaling pathways. Molecular docking and kinetic simulations confirmed stable binding between the targets and B[a]P, with PTPRC exhibiting exceptionally high stability in its interactions. This study elucidated the molecular mechanisms underlying B[a]P-induced eosinophil-related COPD through network toxicology, molecular docking and kinetic modeling. It identified key targets (PTPRC, AKT1, CSF-1R) and elucidated the molecular mechanisms linking environmental pollutants to COPD pathology and the association between environmental pollutants and eosinophil-associated COPD pathology. These findings provide a scientific basis for targeted interventions.
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.