Evidence map›Paper›PMID 23449446›Full record

ArticleCell death & disease2013

Nuclear factor-κB modulates osteogenesis of periodontal ligament stem cells through competition with β-catenin signaling in inflammatory microenvironments.

X Chen, C Hu, G Wang, L Li, X Kong, Y Ding, Y Jin

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05657015 (Lepidium Sativum Extract Versus Simvastatin as an Adjunctive Local Delivery Agents to Non-Surgical Periodontal Therapy), which is not on this map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.6field-weighted citation impact, top 5% of its field
1 · What the graph read from 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.

2 · The registry

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.

NCT05657015 phase4completednot on this mapstarted 2021, after this paper: background citation

Lepidium Sativum Extract Versus Simvastatin as an Adjunctive Local Delivery Agents to Non-Surgical Periodontal Therapy: A Randomized Controlled Clinical Trial With Biochemical Analysis

TypeinterventionalSponsorAin Shams UniversityRan2021 to 2022Enrolled30ConditionsPeriodontitisArmsLepidium Sativum, Simvastatin
3 · Its place in the literature

Who cites it

63 citing papers in PubMed, 127 citations in OpenAlex.

  1. Review
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  4. Article
  5. Investigating the Osteoregenerative Properties ofJournal of functional biomaterials · 2025
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3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

X ChenDepartment of Orthodontics, School of Stomatology, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.
C Hu
G Wang
L Li
X Kong
Y Ding
Y Jin
Air Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation can influence multipotency and self-renewal of mesenchymal stem cells (MSCs), resulting in their awakened bone-regeneration ability. Human periodontal ligament tissue-derived MSCs (PDLSCs) have been isolated, and their differentiation potential was found to be defective due to β-catenin signaling indirectly regulated by inflammatory microenvironments. Nuclear factor-κB (NF-κB) is well studied in inflammation by many different groups. The role of NF-κB needs to be studied in PDLSCs, although genetic evidences have recently shown that NF-κB inhibits osteoblastic bone formation in mice. However, the mechanism as to how inflammation leads to the modulation of β-catenin and NF-κB signaling remains unclear. In this study, we investigated β-catenin and NF-κB signaling through regulation of glycogen synthase kinase 3β activity (GSK-3β, which modulates β-catenin and NF-κB signaling) using a specific inhibitor LiCl and a phosphatidylinositol 3-kinase (PI3K) inhibitor LY 294002. We identified that NF-κB signaling might be more important for the regulation of osteogenesis in PDLSCs from periodontitis compared with β-catenin. BAY 11-7082 (an inhibitor of NF-κB) could inhibit phosphorylation of p65 and partly rescue the differentiation potential of PDLSCs in inflammation. Our data indicate that NF-κB has a central role in regulating osteogenic differentiation of PDLSCs in inflammatory microenvironments. Given the molecular mechanisms of NF-κB in osteogenic differentiation governed by inflammation, it can be said that NF-κB helps in improving stem cell-mediated inflammatory bone disease therapy.

Indexed as

Cellular MicroenvironmentOsteogenesisAdultAnimalsbeta CateninCell DifferentiationCells, CulturedChromonesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansInflammationLithium ChlorideMesenchymal Stem CellsMiceMorpholines2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one3-(4-methylphenylsulfonyl)-2-propenenitrilebeta CateninChromonesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouseLithium ChlorideMorpholinesNF-kappa BNitrilesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsRNA, MessengerSulfonesTranscription Factor RelA

Identifiers

PMID23449446
PMCPMC3734811
OpenAlexW1975166559

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

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.