ArticleJournal of dental sciences2024
TNF-α promotes expression of inflammatory factors by upregulating nicotinamide adenine dinucleotide phosphate oxidase-2 expression in human gingival fibroblasts.
Article in Journal of dental sciences, 2024. 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
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
2 citing papers in PubMed, 3 citations in OpenAlex.
- Long Non-coding RNA TLX1NB Regulates Inflammatory Response in Periodontitis by Interacting With Matrix Metalloproteinase 8.Inflammation · 2026Article
- NOX2 exacerbates periodontitis via JAK2-STAT3-mediated ferroptosis of gingival epithelial cells.Frontiers in immunology · 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
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/purpose: Periodontitis is a chronic infectious disease. The oxidative stress environment can cause or exacerbate the inflammation in periodontitis. Nicotinamide adenine dinucleotide phosphate oxidase (NOX) may be the most important source of reactive oxygen species (ROS) in periodontal tissues. The pathological mechanism of periodontitis may be related to the increased ROS caused by enhanced NOX activity. The purpose was to investigate the effect of tumor necrosis factor (TNF-α) on inflammatory cytokines and ROS, and the role of NOX-2 in human gingival fibroblasts (HGFs). Materials and methods: HGFs were cultured and divided into the normal control group (NC group) and the inflammatory model group (TNF-α group) induced by 10 ng/ml TNF-α. Thereafter, NOX-2 siRNA was used to knock down NOX-2 gene expression. Quantitative real-time PCR was applied to detect Results: The mRNA and protein expression levels of Conclusion: TNF-α promotes the expression of NOX-2 in human gingival fibroblasts and enhances the expression of inflammatory factors and ROS in human gingival fibroblasts through the upregulation of NOX-2 partly.
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.