ArticleToxics2025
Suppression of NOX2-Derived Reactive Oxygen Species (ROS) Reduces Epithelial-to-MesEnchymal Transition Through Blocking SiO
Article in Toxics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- NADPH oxidases in immunometabolism and disease pathology: mechanistic networks, pollutant triggers, and therapeutic frontiers.Cellular & molecular immunology · 2026Review
- Rubiadin-1-methyl ether alleviates bleomycin induced pulmonary fibrosis.Scientific reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
(1) Background: Silicosis, a chronic lung fibrosis disorder triggered by the accumulation of silica dust in the deep lung regions, is characterized by intricate molecular mechanisms. Among these, the NOX2 (NADPH oxidase 2) and JNK (C-Jun N-terminal kinase) signaling pathways play pivotal roles in the progression of pulmonary fibrosis. Despite their significance, the precise mechanisms underlying the crosstalk between these pathways remain largely unexplored. (2) Methods: To unravel these interactions, we examined the interplay between JNK and NOX2 in human epithelial cells subjected to silica dust exposure through in vivo assays, followed by validation using single-cell sequencing. Our findings consistently revealed elevated expression levels of key components from both the JNK signaling pathway and NOX2 in the lungs of silicosis-induced mice and silica-treated human epithelial cells. (3) Results: Notably, the activation of these pathways was linked to increased ROS (reactive oxygen species) production, elevated levels of profibrogenic factors, and diminished cell proliferation in silica-exposed human lung epithelial cells. Further mechanistic analyses demonstrated that JNK signaling amplifies NOX2 expression and ROS production induced by silica exposure, while treatment with the JNK inhibitor SP600125 mitigates these effects. Conversely, overexpression of NOX2 enhanced silica-induced JNK activation and the expression of epithelial-mesenchymal transition (EMT)-related factors, whereas NOX2 knockdown exerted the opposite effect. These results suggest a positive feedback loop between JNK and NOX2 signaling, which may drive EMT in lung epithelial cells following silica exposure. (4) Conclusions: This reciprocal interaction appears to play a critical role in lung epithelial cell damage and the pathogenesis of silicosis, shedding light on the molecular mechanisms underlying profibrogenic disease and offering potential avenues for therapeutic intervention.
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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.