ArticleJournal of dental research2018
Smad6 Methylation Represses NFκB Activation and Periodontal Inflammation.
Article in Journal of dental research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- The Role of DNA Methylation and Histone Modification in Periodontal Disease: A Systematic Review.International journal of molecular sciences · 2020Pooled it
- PRMT1-SFPQ regulates intron retention to control matrix gene expression during craniofacial development.eLife · 2026Article
- Article
- Toll-like receptors in innate immunity and inflammation: from fundamental biology to clinic insights.Immunity & inflammation · 2026Review
- PRMT1 in Health and Disease: Emerging Perspectives From Molecular Mechanisms to Therapeutic Strategies.MedComm · 2025Review
- Review
- MicroRNA-671-5p regulates the inflammatory response of periodontal ligament stem cells via the DUSP8/p38 MAPK pathway.Molecular biology reports · 2024Article
- Akkermansia muciniphila inhibited the periodontitis caused by Fusobacterium nucleatum.NPJ biofilms and microbiomes · 2023Article
- SENP3 deletion promotes M2 macrophage polarization and accelerates wound healing through smad6/IκB/p65 signaling pathway.Heliyon · 2023Article
- Transcriptomic analysis of the innate immune response toMolecular therapy. Nucleic acids · 2023Article
- Metformin ameliorates HMGB1-mediated oxidative stress through mTOR pathway in experimental periodontitis.Genes & diseases · 2023Article
- How Protein Methylation Regulates Steroid Receptor Function.Endocrine reviews · 2022Review
- Emerging role of epigenetic regulations in periodontitis: a literature review.American journal of translational research · 2022Review
- Structure, Activity, and Function of PRMT1.Life (Basel, Switzerland) · 2021Review
- Effects of chronic apical periodontitis on the inflammatory response of the aorta in hyperlipemic rats.Clinical oral investigations · 2021Article
- Polymicrobial communities in periodontal disease: Their quasi-organismal nature and dialogue with the host.Periodontology 2000 · 2021Review
- SMAD6 transduces endothelial cell flow responses required for blood vessel homeostasis.Angiogenesis · 2021Article
- Alterations of Asymmetric Dimethylarginine (ADMA)-Containing Protein Profiles Associated with Chronic Pancreatitis Pathogenesis.Journal of inflammation research · 2021Article
- A new anabolic compound, LLP2A-Ale, reserves periodontal bone loss in mice through augmentation of bone formation.BMC pharmacology & toxicology · 2020Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
The balance between pro- and anti-inflammatory signals maintains tissue homeostasis and defines the outcome of chronic inflammatory diseases such as periodontitis, a condition that afflicts the tooth-supporting tissues and exerts an impact on systemic health. The induction of tissue inflammation relies heavily on Toll-like receptor (TLR) signaling, which drives a proinflammatory pathway through recruiting myeloid differentiation primary response gene 88 (MyD88) and activating nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB). TLR-induced production of proinflammatory cytokines and chemokines is reined in by anti-inflammatory cytokines, including the transforming growth factor β (TGFβ) family of cytokines. Although Smad6 is a key mediator of TGFβ-induced anti-inflammatory signaling, the exact mechanism by which TGFβ regulates TLR proinflammatory signaling in the periodontal tissue has not been addressed to date. In this study, we demonstrate for the first time that the ability of TGFβ to inhibit TLR-NFκB signaling is mediated by protein arginine methyltransferase 1 (PRMT1)-induced Smad6 methylation. Upon methylation, Smad6 recruited MyD88 and promoted MyD88 degradation, thereby inhibiting NFκB activation. Most important, Smad6 is expressed and methylated in the gingival epithelium, and PRMT1-Smad6 signaling promotes tissue homeostasis by limiting inflammation. Consistent with this, disturbance of Smad6 methylation exacerbates inflammation and bone loss in experimental periodontitis. The dissected mechanism is therapeutically important, as it highlights the manipulation of PRMT1-Smad6 signaling as a novel promising strategy to modulate the host immune response in periodontitis.
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.