ArticleOral diseases2020
Overactivation of the NF-κB pathway impairs molar enamel formation.
Article in Oral diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Implant-supported fixed prosthodontic treatment for ectodermal dysplasia: a case report.BMC oral health · 2026Article
- Ectodermal dysplasia: a narrative review of the clinical and biological aspects relevant to oral health.Frontiers in pediatrics · 2025Review
- Transcriptome analysis identifies EDA1 variants disrupt FOSB-mediated regulation of odontogenic epithelial cell behaviors during dental germ development.Frontiers in cell and developmental biology · 2025Article
- KDF1 promotes ameloblast differentiation by inhibiting the IKK/IκB/NF-κB axis.Journal of cellular physiology · 2024Article
- The EDA/EDAR/NF-κB pathway in non-syndromic tooth agenesis: A genetic perspective.Frontiers in genetics · 2023Review
- The synergistic effects of TGF-β1 and RUNX2 on enamel mineralization through regulating ODAPH expression during the maturation stage.Journal of molecular histology · 2022Article
- Article
- [Detection ofBeijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2020Article
Corrections and comments
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Authors and funding
20 authors at 7 institutions in 5 countries.
Funding
Abstract
objectiveHypohidrotic ectodermal dysplasia (HED) is a hereditary disorder characterized by abnormal structures and functions of the ectoderm-derived organs, including teeth. HED patients exhibit a variety of dental symptoms, such as hypodontia. Although disruption of the EDA/EDAR/EDARADD/NF-κB pathway is known to be responsible for HED, it remains unclear whether this pathway is involved in the process of enamel formation. EXPERIMENTAL SUBJECTS AND
methodsTo address this question, we examined the mice overexpressing Ikkβ (an essential component required for the activation of NF-κB pathway) under the keratin 5 promoter (K5-Ikkβ).
resultsUpregulation of the NF-κB pathway was confirmed in the ameloblasts of K5-Ikkβ mice. Premature abrasion was observed in the molars of K5-Ikkβ mice, which was accompanied by less mineralized enamel. However, no significant changes were observed in the enamel thickness and the pattern of enamel rods in K5-Ikkβ mice. Klk4 expression was significantly upregulated in the ameloblasts of K5-Ikkβ mice at the maturation stage, and the expression of its substrate, amelogenin, was remarkably reduced. This suggests that abnormal enamel observed in K5-Ikkβ mice was likely due to the compromised degradation of enamel protein at the maturation stage.
conclusionTherefore, we could conclude that the overactivation of the NF-κB pathway impairs the process of amelogenesis.
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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.