ArticleJournal of thoracic disease2024
Regulatory mechanisms of haptoglobin on particulate matter-induced epithelial-to-mesenchymal transition in bronchial epithelial cells.
Article in Journal of thoracic disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: It has been proposed that repeated exposure of bronchial epithelial cells to atmospheric particulate matter (PM) could disrupt airway epithelial integrity and lead to epithelial-to-mesenchymal transition (EMT) and ultimately airway remodeling. The molecular mechanisms underlying PM-related bronchial epithelial EMT have not yet been elucidated. The aim of this research is to clarify the molecular mechanism of EMT upon PM exposure. Methods: Using an Results: Conclusions: HP is an important mediator of PM-induced EMT in bronchial epithelial cells and promotes PM-induced EMT in bronchial epithelial cells through activation of the STAT3 signaling pathway and the ERK signaling pathway. Inhibition of HP expression attenuates PM exposure-induced EMT in bronchial epithelial cells.
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Registered trials
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