ArticleAmerican journal of physiology. Heart and circulatory physiology2012
Acute O-GlcNAcylation prevents inflammation-induced vascular dysfunction.
Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Adjuvant therapies for management of hemorrhagic shock: a narrative review.Critical care (London, England) · 2025Pooled it
- O-GlcNAcylation: A molecular switch linking brain health to neurodegeneration.Neural regeneration research · 2026Article
- Post-translational modification gene signatures implicate FBXW7 in immune and vascular dysregulation of Moyamoya disease.Frontiers in genetics · 2025Article
- Thiamet-G facilitates reparative dentin formation via modulating O-GlcNAcylation and inflammation.Frontiers in physiology · 2025Article
- Decoding glycosylation in cardiovascular diseases: mechanisms, biomarkers, and therapeutic opportunities.Frontiers in pharmacology · 2025Review
- Post-translational modifications of pyruvate dehydrogenase complex in cardiovascular disease.iScience · 2024Review
- O-GlcNAcylation of NLRP3 Contributes to Lipopolysaccharide-Induced Pyroptosis of Human Gingival Fibroblasts.Molecular biotechnology · 2024Article
- Protein glycosylation in cardiovascular health and disease.Nature reviews. Cardiology · 2024Review
- Roles of O-GlcNAcylation in Mitochondrial Homeostasis and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- O-GlcNAcylation: a pro-survival response to acute stress in the cardiovascular and central nervous systems.European journal of medical research · 2024Review
- O-GlcNAc modification of GSDMD attenuates LPS-induced endothelial cells pyroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- The O-GlcNAc dichotomy: when does adaptation become pathological?Clinical science (London, England : 1979) · 2023Review
- The Glycobiology of Pulmonary Arterial Hypertension.Metabolites · 2022Review
- Article
- Targeting ProteinCells · 2022Review
- The dual role of the hexosamine biosynthetic pathway in cardiac physiology and pathophysiology.Frontiers in endocrinology · 2022Review
- Role of Posttranslational Modifications of Proteins in Cardiovascular Disease.Oxidative medicine and cellular longevity · 2022Review
- Laminar Flow on Endothelial Cells Suppresses eNOS O-GlcNAcylation to Promote eNOS Activity.Circulation research · 2021Article
- O‑GlcNAcylation contributes to intermittent hypoxia‑associated vascular dysfunction via modulation of MAPKs but not CaMKII pathways.Molecular medicine reports · 2021Article
- Remote Ischemic Perconditioning Ameliorates Myocardial Ischemia and Reperfusion-Induced Coronary Endothelial Dysfunction and Aortic Stiffness in Rats.Journal of cardiovascular pharmacology and therapeutics · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Acute increases in cellular protein O-linked N-acetyl-glucosamine (O-GlcNAc) modification (O-GlcNAcylation) have been shown to have protective effects in the heart and vasculature. We hypothesized that d-glucosamine (d-GlcN) and Thiamet-G, two agents that increase protein O-GlcNAcylation via different mechanisms, inhibit TNF-α-induced oxidative stress and vascular dysfunction by suppressing inducible nitric oxide (NO) synthase (iNOS) expression. Rat aortic rings were incubated for 3h at 37°C with d-GlcN or its osmotic control l-glucose (l-Glc) or with Thiamet-G or its vehicle control (H(2)O) followed by the addition of TNF-α or vehicle (H(2)O) for 21 h. After incubation, rings were mounted in a myograph to assess arterial reactivity. Twenty-four hours of incubation of aortic rings with TNF-α resulted in 1) a hypocontractility to 60 mM K(+) solution and phenylephrine, 2) blunted endothelium-dependent relaxation responses to ACh and substance P, and 3) unaltered relaxing response to the Ca(2+) ionophore A-23187 and the NO donor sodium nitroprusside compared with aortic rings cultured in the absence of TNF-α. d-GlcN and Thiamet-G pretreatment suppressed the TNF-α-induced hypocontractility and endothelial dysfunction. Total protein O-GlcNAc levels were significantly higher in aortic segments treated with d-GlcN or Thiamet-G compared with controls. Expression of iNOS protein was increased in TNF-α-treated rings, and this was attenuated by pretreatment with either d-GlcN or Thiamet-G. Dense immunostaining for nitrotyrosylated proteins was detected in the endothelium and media of the aortic wall, suggesting enhanced peroxynitrite production by iNOS. These findings demonstrate that acute increases in protein O-GlcNAcylation prevent TNF-α-induced vascular dysfunction, at least in part, via suppression of iNOS expression.
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Registered trials
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