ArticleFrontiers in pharmacology2025
O-GlcNAcylation of eNOS in high-salt-induced thoracic aorta endothelial dysfunction in mice.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Glycosylation modification: a trigger for obesity and its complications?Molecular medicine (Cambridge, Mass.) · 2026Review
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4 authors.
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Abstract
Background: Excessive salt intake is a well-established risk factor for hypertension. However, the molecular mechanisms by which salt-induced endothelial dysfunction contributes to blood pressure elevation remain incompletely understood. Methods and Results: In this study, mice were fed a normal-salt diet (NSD) or high-salt diet (HSD) for 4 weeks, and primary bovine aortic endothelial cells (BAECs) were treated with varying concentrations of NaCl. HSD mice showed increased diastolic blood pressure and impaired acetylcholine-induced vasodilation, while sodium nitroprusside responses remained intact. Conclusion: Our findings suggest that high salt intake impairs endothelial function by enhancing O-GlcNAc of eNOS, thereby contributing to elevated diastolic blood pressure. The ability of OGT inhibition to reverse endothelial dysfunction highlights the therapeutic potential of targeting eNOS O-GlcNAc could be a promising approach for preventing salt-induced vascular damage and subsequent diastolic blood pressure elevation.
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