ArticleFrontiers in immunology2026
NOX2 exacerbates periodontitis via JAK2-STAT3-mediated ferroptosis of gingival epithelial cells.
Article in Frontiers in immunology, 2026. 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.
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Who cites it
2 citing papers in PubMed.
- HIPK2 mediated regulation of ferroptosis and inflammatory signaling in sepsis-induced myocardial injury.Journal of molecular histology · 2026Article
- The macrophage polarization-ferroptosis axis as a therapeutically targetable immunometabolic framework in periodontitis.Frontiers in immunology · 2026Review
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Authors and funding
8 authors.
Funding
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Abstract
Background: Ferroptosis is a novel form of regulated cell death driven by lipid peroxidation and oxidative stress, and has been implicated in the pathogenesis of periodontitis. The purpose of this study was to elucidate mechanisms by which NADPH oxidase 2 (NOX2) promotes ferroptosis in gingival epithelial cells and contributes to periodontitis Methods: Periodontitis was induced in C57BL/6 mice by silk ligation and an Results: NOX2 expression was significantly elevated in the gingival tissues of periodontitis patients, the mouse model and Pg-LPS-stimulated CA9-22 cells. Mechanistically, we confirmed that Pg-LPS upregulated NOX2 by triggering the TLR4/NF-κB pathway. Gene silencing of NOX2 Conclusions: NOX2 activation promoted periodontitis by driving ferroptosis via the ROS/JAK2-STAT3 pathway, highlighting its potential as a novel therapeutic target.
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