ArticleAmerican journal of physiology. Cell physiology2015
O-GlcNAcase overexpression reverses coronary endothelial cell dysfunction in type 1 diabetic mice.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 54 citations in OpenAlex.
- Pathogenesis of diabetic cardiomyopathy and emerging therapeutic strategies: a network-based perspective.Frontiers in clinical diabetes and healthcare · 2026Review
- O-GlcNAcylation in diabetic cardiac remodeling and a proposed endothelial-macrophage-fibroblast network.Frontiers in immunology · 2026Review
- Protein O-GlcNAcylation and hexokinase mitochondrial dissociation drive heart failure with preserved ejection fraction.Cell metabolism · 2025Article
- O-linked β-N-acetylglucosamine modification in diabetic foot ulcer pathogenesis.Burns & trauma · 2025Review
- The O-GlcNAc dichotomy: when does adaptation become pathological?Clinical science (London, England : 1979) · 2023Review
- Best practices in assessing cardiac proteinAmerican journal of physiology. Heart and circulatory physiology · 2023Article
- The Protective Effect of 11-Keto-β-Boswellic Acid against Diabetic Cardiomyopathy in Rats Entails Activation of AMPK.Nutrients · 2023Article
- Connexins and Glucose Metabolism in Cancer.International journal of molecular sciences · 2022Review
- Review
- O-Linked β-Frontiers in immunology · 2022Review
- Understanding diabetes-induced cardiomyopathy from the perspective of renin angiotensin aldosterone system.Pflugers Archiv : European journal of physiology · 2022Review
- Glycation and Glycosylation in Cardiovascular Remodeling: Focus on Advanced Glycation End Products and O-Linked Glycosylations as Glucose-Related Pathogenetic Factors and Disease Markers.Journal of clinical medicine · 2021Review
- The Mystery of Diabetic Cardiomyopathy: From Early Concepts and Underlying Mechanisms to Novel Therapeutic Possibilities.International journal of molecular sciences · 2021Review
- Reduced reticulum-mitochondria CaBasic research in cardiology · 2020Article
- O-GlcNAcylation Mediates Glucose-Induced Alterations in Endothelial Cell Phenotype in Human Diabetes Mellitus.Journal of the American Heart Association · 2020Article
- Overexpression of p53 due to excess protein O-GlcNAcylation is associated with coronary microvascular disease in type 2 diabetes.Cardiovascular research · 2020Article
- Chloroquine differentially modulates coronary vasodilation in control and diabetic mice.British journal of pharmacology · 2020Article
- Metabolic Stress and Cardiovascular Disease in Diabetes Mellitus: The Role of ProteinArteriosclerosis, thrombosis, and vascular biology · 2019Review
- Endothelium-Dependent Hyperpolarization (EDH) in Diabetes: Mechanistic Insights and Therapeutic Implications.International journal of molecular sciences · 2019Review
- Pulmonary vascular dysfunction in metabolic syndrome.The Journal of physiology · 2019Review
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9 authors at 3 institutions in 1 country.
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Abstract
Cardiovascular disease is the primary cause of morbidity and mortality in diabetes, and endothelial dysfunction is commonly seen in these patients. Increased O-linked N-acetylglucosamine (O-GlcNAc) protein modification is one of the central pathogenic features of diabetes. Modification of proteins by O-GlcNAc (O-GlcNAcylation) is regulated by two key enzymes: β-N-acetylglucosaminidase [O-GlcNAcase (OGA)], which catalyzes the reduction of protein O-GlcNAcylation, and O-GlcNAc transferase (OGT), which induces O-GlcNAcylation. However, it is not known whether reducing O-GlcNAcylation can improve endothelial dysfunction in diabetes. To examine the effect of endothelium-specific OGA overexpression on protein O-GlcNAcylation and coronary endothelial function in diabetic mice, we generated tetracycline-inducible, endothelium-specific OGA transgenic mice, and induced OGA by doxycycline administration in streptozotocin-induced type 1 diabetic mice. OGA protein expression was significantly decreased in mouse coronary endothelial cells (MCECs) isolated from diabetic mice compared with control MCECs, whereas OGT protein level was markedly increased. The level of protein O-GlcNAcylation was increased in diabetic compared with control mice, and OGA overexpression significantly decreased the level of protein O-GlcNAcylation in MCECs from diabetic mice. Capillary density in the left ventricle and endothelium-dependent relaxation in coronary arteries were significantly decreased in diabetes, while OGA overexpression increased capillary density to the control level and restored endothelium-dependent relaxation without changing endothelium-independent relaxation. We found that connexin 40 could be the potential target of O-GlcNAcylation that regulates the endothelial functions in diabetes. These data suggest that OGA overexpression in endothelial cells improves endothelial function and may have a beneficial effect on coronary vascular complications in diabetes.
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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.