ArticleJournal of oral biology and craniofacial research
Overexpression of insulin-like growth factor-2 mRNA-binding protein 1 is associated with periodontal disease.
Article in Journal of oral biology and craniofacial research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The Central Role of m6A as Epigenetic Regulator in Metabolic Disorders of Therapeutic Potential and Clinical Implications.Molecular neurobiology · 2025Review
- N6-Methyladenosine Modification of the Three Components "Writers", "Erasers", and "Readers" in Relation to Osteogenesis.International journal of molecular sciences · 2025Review
- N6-methyladenosine-mediated overexpression of TREM-1 is associated with periodontal disease.Odontology · 2025Article
- Evaluation of the relationship between subgingival microbiome in obese and nonobese clinically healthy and periodontitis patients - An experimental study.Journal of Indian Society of PeriodontologyArticle
- E-cigarette aerosol exposure drives extracellular matrix gene dysregulation and collagen remodeling in gingival fibroblasts: AnJournal of oral biology and craniofacial researchArticle
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Authors and funding
5 authors.
Funding
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Abstract
Objective: To investigate the potential role of a novel m6A RNA regulator, Insulin-like Growth Factor-2 mRNA-binding protein 1 (IGF2BP1), in periodontal disease pathogenesis. Materials and methods: Gingival tissue samples from 60 periodontitis patients and 60 healthy individuals were analyzed for IGF2BP1 mRNA and protein expression Results: IGF2BP1 mRNA and protein levels were significantly higher in the periodontitis group compared to the healthy group. Functional analysis implicated IGF2BP1 in regulating the IL-17 signaling pathway, a key player in inflammation. Pg-LPS treatment upregulated IGF2BP1 and proinflammatory cytokines in HGFs, supporting this finding. Conclusion: Our study suggests that IGF2BP1 overexpression contributes to periodontitis pathogenesis, potentially through IL-17 signaling. Further research is needed to elucidate the precise molecular mechanisms and explore IGF2BP1 as a potential therapeutic target or biomarker for this common oral disease.
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