ArticleBioengineered2022
Long non-coding RNA ZFY-AS1 represses periodontitis tissue inflammation and oxidative damage via modulating microRNA-129-5p/DEAD-Box helicase 3 X-linked axis.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 8 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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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
8 citing papers in PubMed, 10 citations in OpenAlex.
- E3 ubiquitin ligase trim36 targets ddx3x for degradation to reprogram macrophage polarization and ameliorate tubal factor infertility in rats.Cell biology and toxicology · 2026Article
- The expression profile and clinical relevance of miR-125a-5p in individuals with chronic periodontitis.Acta odontologica Scandinavica · 2026Article
- Noncoding RNAs in periodontitis: Progress and perspectives (Review).International journal of molecular medicine · 2025Review
- A Transcriptomic Approach to Sex Differences in Calcific Aortic Valve Stenosis in Patients with a Tricuspid Aortic Valve.CJC open · 2025Article
- Epigenetic factors associated with peri-implantitis: a review.Journal of Zhejiang University. Science. B · 2025Review
- Article
- Review
- Exosomal miR-205-5p derived from periodontal ligament stem cells attenuates the inflammation of chronic periodontitis via targeting XBP1.Immunity, inflammation and disease · 2023Article
Corrections and comments
- Retracted
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A large number of studies have manifested long non-coding RNA (lncRNA) is involved in the modulation of the development of periodontitis, but the specific mechanism has not been fully elucidated. The purpose of this study was to explore the biological function and latent molecular mechanism of lncZFY-AS1 in periodontitis. The results clarified lncZFY-AS1 and DEAD-Box Helicase 3 X-Linked (DDX3X) were up-regulated, but microRNA (miR)-129-5p was down-regulated in periodontitis. Knockdown of lncZFY-AS2 or overexpression of miR-129-5p decreased macrophage infiltration and periodontal membrane cell apoptosis, increased cell viability, repressed inflammatory factors and nuclear factor kappa B activation, reduced oxidative stress, but promoted nuclear factor-E2-related factor 2/heme oxygenase 1 expression. LncZFY-AS1 elevation further aggravated periodontitis inflammation, oxidative stress, and apoptosis. LncZFY competitively adsorbed miR-129-5p to mediate DDX3X expression. Knockdown lncZFY's improvement effect on periodontitis was reversed by depressive miR-129-5p or enhancive DDX3X. In conclusion, these data suggest lncZFY-AS1 promotes inflammatory injury and oxidative stress in periodontitis by competitively binding to miR-129-5p and mediating DDX3X expression. LncZFY-AS1/miR-129-5p/DDX3X may serve as a novel molecular target for treatment of periodontitis in the future.
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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.