ArticleDrug design, development and therapy2026
Semaglutide Inhibits Osteoblast Ferroptosis Induced by Diabetic Periodontitis via Modulating the Wnt5a/Ror2/p38 MAPK Signaling Pathway.
Article in Drug design, development and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- Semaglutide in Diabetic Periodontitis-Induced Osteoblast Ferroptosis: Pharmacological and Methodological Insights [Letter].Drug design, development and therapy · 2026Article
- Response to "Semaglutide in Diabetic Periodontitis-Induced Osteoblast Ferroptosis: Pharmacological and Methodological Insights" [Response to Letter].Drug design, development and therapy · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Type 2 diabetes mellitus (T2DM) is a major risk factor for periodontitis, often leading to exacerbated alveolar bone loss. Ferroptosis, an iron-dependent regulated cell death pathway, contributes to osteoblast dysfunction under diabetic conditions. The non-canonical Wnt5a/Ror2 pathway is pivotal in inflammation and bone metabolism. Semaglutide, a long-acting GLP-1 receptor agonist, may modulate this pathway and protect osteoblasts from ferroptosis, however, its role in diabetic periodontitis remains unclear. Methods: MC3T3-E1 osteoblasts were exposed to high glucose plus palmitic acid (HGHP) to mimic a diabetic microenvironment. The effects of Semaglutide on osteoblast proliferation, migration, differentiation, mineralization, and ferroptosis were assessed using EDU, Transwell, ALP and ARS staining, qPCR, Western blotting, ROS, Fe Results: HGHP induced osteoblast ferroptosis, increased oxidative stress, and impaired osteogenic function. Semaglutide restored proliferation and osteogenic capacity and attenuated oxidative stress and ferroptosis. Wnt5a was upregulated by HGHP; its silencing reduced ferroptosis and improved osteogenesis. Semaglutide suppressed HGHP-induced Wnt5a/Ror2/p38 MAPK activation, whereas p38 activation blunted its protective effects. In T2DM periodontitis mice, semaglutide reduced periodontal inflammation and osteoblast ferroptosis. Conclusion: Semaglutide mitigates HGHP-induced osteoblast ferroptosis and improves osteogenic function via the Wnt5a/Ror2/p38 MAPK pathway, supporting its potential in diabetic periodontitis.
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