ReviewCardiovascular research2007
Role of protein O-linked N-acetyl-glucosamine in mediating cell function and survival in the cardiovascular system.
Review in Cardiovascular research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 2 of them syntheses that pooled it.
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
80 citing papers in PubMed, 2 syntheses or guidelines pooled it, 163 citations in OpenAlex.
- The effect of acarbose on inflammatory cytokines and adipokines in adults: a systematic review and meta-analysis of randomized clinical trials.Inflammopharmacology · 2024Pooled it
- Implications of Diabetes-Induced Altered Metabolites on Retinal Neurodegeneration.Frontiers in neuroscience · 2022Pooled it
- Effect of acarbose on platelet-derived microparticles, soluble selectins, and adiponectin in diabetic patients.Journal of thrombosis and thrombolysis · 2009Trial
- Renal-Cardiac Crosstalk in the Pathogenesis and Progression of Heart Failure.Circulation research · 2025Review
- Review
- Isthmin-1 Improves Aging-Related Cardiac Dysfunction in Mice through Enhancing Glycolysis and SIRT1 Deacetylase Activity.Aging and disease · 2024Article
- O-GlcNAc modification of GSDMD attenuates LPS-induced endothelial cells pyroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Endothelial Dysfunction in Obesity and Therapeutic Targets.Advances in experimental medicine and biology · 2024Review
- The O-GlcNAc dichotomy: when does adaptation become pathological?Clinical science (London, England : 1979) · 2023Review
- Acute stress induces long-term metabolic, functional, and structural remodeling of the heart.Nature communications · 2023Article
- O-GlcNAcylation: an important post-translational modification and a potential therapeutic target for cancer therapy.Molecular medicine (Cambridge, Mass.) · 2022Review
- Protein O-GlcNAcylation and the regulation of energy homeostasis: lessons from knock-out mouse models.Journal of biomedical science · 2022Review
- Recent Advances on Drug Development and Emerging Therapeutic Agents Through Targeting Cellular Homeostasis for Ageing and Cardiovascular Disease.Frontiers in aging · 2022Review
- Cardiovascular Benefits from Gliflozins: Effects on Endothelial Function.Biomedicines · 2021Review
- Cardio-Oncology: Understanding the Intersections Between Cardiac Metabolism and Cancer Biology.JACC. Basic to translational science · 2021Review
- Hypertonic stress modulates eNOS function through O-GlcNAc modification at Thr-866.Scientific reports · 2021Article
- Role ofPhysiological reviews · 2021Review
- O-GlcNAcylation Mediates Glucose-Induced Alterations in Endothelial Cell Phenotype in Human Diabetes Mellitus.Journal of the American Heart Association · 2020Article
- Very Low-Density Lipoproteins of Metabolic Syndrome Modulates STIM1, Suppresses Store-Operated Calcium Entry, and Deranges Myofilament Proteins in Atrial Myocytes.Journal of clinical medicine · 2019Article
- Nutrient regulation of signaling and transcription.The Journal of biological chemistry · 2019Review
20 more citing papers are in PubMed but not listed here.
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 1 institution in 1 country.
Funding
Abstract
There is growing recognition that the O-linked attachment of N-acetyl-glucosamine (O-GlcNAc) on serine and threonine residues of nuclear and cytoplasmic proteins is a highly dynamic post-translational modification that plays a key role in signal transduction pathways. Numerous proteins have been identified as targets of O-GlcNAc modifications including kinases, phosphatases, transcription factors, metabolic enzymes, chaperons, and cytoskeletal proteins. Modulation of O-GlcNAc levels has been shown to modify DNA binding, enzyme activity, protein-protein interactions, the half-life of proteins, and subcellular localization. The level of O-GlcNAc is regulated in part by the metabolism of glucose via the hexosamine biosynthesis pathway (HBP), and the metabolic abnormalities associated with insulin resistance and diabetes, such as hyperglycemia, hyperlipidemia, and hyperinsulinemia, are all associated with increased flux through the HBP and elevated O-GlcNAc levels. Increased HBP flux and O-GlcNAc levels have been implicated in the impaired relaxation of isolated cardiomyocytes, blunted response to angiotensin II and phenylephrine, hyperglycemia-induced cardiomyocyte apoptosis, and endothelial and vascular cell dysfunction. In contrast to these adverse effects, recent studies have also shown that O-GlcNAc levels increase in response to acute stress and that this is associated with increased cell survival. Thus, while the relationship between O-GlcNAc levels and cellular function is complex and not well-understood, it is clear that these pathways play a critical role in the regulation of cell function and survival in the cardiovascular system and may be implicated in the adverse effects of metabolic disease on the heart.
Indexed as
Identifiers
What OpenQuestion holds
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.