ReviewLife sciences2013
Post-translational protein modification by O-linked N-acetyl-glucosamine: its role in mediating the adverse effects of diabetes on the heart.
Review in Life sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 77 citations in OpenAlex.
- CHCHD3(MIC19): mitochondrial cristae structure regulation and disease associations.Frontiers in molecular biosciences · 2026Review
- PERM1 Gene Delivery via AAV Prevents Heart Failure in a Mouse Model of Pressure Overload.bioRxiv : the preprint server for biology · 2025Article
- PERM1 regulates mitochondrial energetics through O-GlcNAcylation in the heart.Journal of molecular and cellular cardiology · 2025Article
- Role of Circulating Biomarkers in Diabetic Cardiomyopathy.Biomedicines · 2024Review
- Update on clinical and experimental management of diabetic cardiomyopathy: addressing current and future therapy.Frontiers in endocrinology · 2024Review
- Direct regulation of the cardiac ryanodine receptor (RyR2) by O-GlcNAcylation.Cardiovascular diabetology · 2023Article
- Tacrolimus Improves Therapeutic Efficacy of Umbilical Cord Blood-Derived Mesenchymal Stem Cells in Diabetic Retinopathy by Suppressing DRP1-Mediated Mitochondrial Fission.Antioxidants (Basel, Switzerland) · 2023Article
- ProteinMetabolites · 2022Review
- Dietary Fructose and Fructose-Induced Pathologies.Annual review of nutrition · 2022Review
- Normalizing glucose levels reconfigures the mammary tumor immune and metabolic microenvironment and decreases metastatic seeding.Cancer letters · 2021Article
- NADH/NADBiomolecules · 2021Review
- Role of O-linked N-acetylglucosamine (O-GlcNAc) modification of proteins in diabetic cardiovascular complications.Current opinion in pharmacology · 2021Review
- Role ofPhysiological reviews · 2021Review
- Glycolytic Metabolism, Brain Resilience, and Alzheimer's Disease.Frontiers in neuroscience · 2021Review
- Fructose Metabolism and Cardiac Metabolic Stress.Frontiers in pharmacology · 2021Review
- Defining the Progression of Diabetic Cardiomyopathy in a Mouse Model of Type 1 Diabetes.Frontiers in physiology · 2020Article
- Cardiomyocyte Oga haploinsufficiency increases O-GlcNAcylation but hastens ventricular dysfunction following myocardial infarction.PloS one · 2020Article
- Article
- GRP78 translocation to the cell surface and O-GlcNAcylation of VE-Cadherin contribute to ER stress-mediated endothelial permeability.Scientific reports · 2019Article
- E2f1 deletion attenuates infarct-induced ventricular remodeling without affecting O-GlcNAcylation.Basic research in cardiology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The post-translation attachment of O-linked N-acetylglucosamine, or O-GlcNAc, to serine and threonine residues of nuclear and cytoplasmic proteins is increasingly recognized as a key regulator of diverse cellular processes. O-GlcNAc synthesis is essential for cell survival and it has been shown that acute activation of pathways, which increase cellular O-GlcNAc levels is cytoprotective; however, prolonged increases in O-GlcNAcylation have been implicated in a number of chronic diseases. Glucose metabolism via the hexosamine biosynthesis pathway plays a central role in regulating O-GlcNAc synthesis; consequently, sustained increases in O-GlcNAc levels have been implicated in glucose toxicity and insulin resistance. Studies on the role of O-GlcNAc in regulating cardiomyocyte function have grown rapidly over the past decade and there is growing evidence that increased O-GlcNAc levels contribute to the adverse effects of diabetes on the heart, including impaired contractility, calcium handling, and abnormal stress responses. Recent evidence also suggests that O-GlcNAc plays a role in epigenetic control of gene transcription. The goal of this review is to provide an overview of our current knowledge about the regulation of protein O-GlcNAcylation and to explore in more detail O-GlcNAc-mediated responses in the diabetic heart.
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Registered trials
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.