ArticleWorld journal of diabetes2025
O-linked β-N-acetylglucosamine transferase regulates macrophage polarization in diabetic periodontitis:
Article in World journal of diabetes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Combined Effects of Puerarin and Adipose-Derived Stem Cells on Alveolar Bone Preservation and Inflammation Control in Periodontitis Through p38MAPK Modulation.The Kaohsiung journal of medical sciences · 2026Article
- Discovery of Sennoside A as a NaturalResearch (Washington, D.C.) · 2026Article
- Protein O-GlcNAcylation in Health and Diseases.MedComm · 2025Review
- Review
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Authors and funding
9 authors.
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Abstract
backgroundPeriodontitis, when exacerbated by diabetes, is characterized by increased M1 macrophage polarization and decreased M2 polarization. O-linked β-N-acetylglucosamine (O-GlcNAcylation), catalyzed by O-GlcNAc transferase (OGT), promotes inflammatory responses in diabetic periodontitis (DP). Additionally, p38 mitogen-activated protein kinase regulates macrophage polarization. However, the interplay between OGT, macrophage polarization, and p38 signaling in the progression of DP remains unexplored.
aimTo investigate the effect of OGT on macrophage polarization in DP and its role in mediating O-GlcNAcylation of p38.
methodsFor
resultsOur results demonstrated that M1 macrophage polarization led to maxillary bone loss in DP mice, associated with elevated O-GlcNAcylation and OGT levels. Knockdown of OGT promoted the shift from M1 to M2 macrophage polarization in both mouse periodontal tissues and LPS + HG-induced RAW264.7 cells. Furthermore, LPS + HG enhanced the O-GlcNAcylation of p38 in RAW264.7 cells. OGT interacted with p38 to promote its O-GlcNAcylation at residues A28, T241, and T347, as well as its phosphorylation at residue Y221.
conclusionInhibition of OGT-mediated p38 O-GlcNAcylation deactivates the p38 pathway by suppressing its self-phosphorylation, thereby promoting M1 to M2 macrophage polarization and mitigating DP. These findings suggested that modulating macrophage polarization through regulation of O-GlcNAcylation may represent a novel therapeutic strategy for treating DP.
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