Evidence map›Paper›PMID 41653834›Full record

ArticleInternational dental journal2026

Fut8-Mediated Core Fucosylation of Toll-Like Receptor 4 Exacerbates Periodontitis Via Hyperactivation of NF-κB Signalling.

Jiahao Lin, Yongxi Luo, Lu Chen, Cheng Zeng, Lu Wang, Xinmiao Luo, Li Zeng, Huiyong Xu, Zhao Chen

Abstract read
In one paragraph

Article in International dental journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Jiahao LinDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, PR China.
Yongxi LuoDepartment of Stomatology, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, PR China; Department of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, PR China.
Lu ChenDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, PR China.
Cheng ZengDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, PR China.
Lu WangDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, PR China.
Xinmiao LuoDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, PR China.
Li ZengDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, PR China.
Huiyong XuDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, PR China. Electronic address: xuhuiyong@i.smu.edu.cn.
Zhao ChenDepartment of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, PR China. Electronic address: tinycozy@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic inflammation in periodontitis is linked to aberrant glycosylation, yet the molecular mechanisms and therapeutic potential of the core fucosyltransferase Fut8 remain undefined.

methodsGingival samples from healthy individuals and periodontitis patients were collected. Glycosylation levels were assessed using histological and molecular biological techniques. A mouse periodontitis model was established and injected with the core fucosylation inhibitor 2FF. Integrated transcriptomic and single-cell sequencing data were analysed to screen for key molecules. An in vitro human gingival fibroblast model was utilized. Gene silencing, coimmunoprecipitation, and pathway analysis were employed to elucidate the Fut8-Toll-like receptor 4 (TLR4) regulatory mechanism.

resultsCore fucosylation levels were significantly elevated in periodontitis tissues. Inhibiting this modification alleviated gingival inflammation and bone resorption. Single-cell analysis identified fibroblasts as having the highest glycosylation activity, and Fut8 was pinpointed as the central regulatory molecule. Fut8 enhanced the sensitivity of the NF-κB pathway by mediating glycosylation of TLR4. Silencing Fut8 significantly suppressed inflammatory cytokine secretion. Dual-gene silencing confirmed that Fut8 and TLR4 synergistically drive the inflammatory cascade.

conclusionFut8 amplifies NF-κB signalling through core fucosylation of TLR4. Targeted inhibition of Fut8 blocks periodontal tissue destruction, providing a theoretical basis for glycosylation-targeted therapy. CLINICAL RELEVANCE: Targeting Fut8-mediated core fucosylation offers a promising therapeutic strategy to suppress inflammation and halt tissue destruction in periodontitis.

Indexed as

FucoseFucosyltransferasesNF-kappa BPeriodontitisToll-Like Receptor 4AnimalsDisease Models, AnimalFemaleFibroblastsGlycosylationHumansMaleMiceMice, Inbred C57BLSignal TransductionFucoseFucosyltransferasesNF-kappa BTLR4 protein, humanToll-Like Receptor 4Core fucosylationFut8GlycosylationPeriodontitisTLR4

Identifiers

PMID41653834
PMCPMC12907083

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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.