ReviewCells2019
Hyperglycemia-Induced Aberrant Cell Proliferation; A Metabolic Challenge Mediated by Protein O-GlcNAc Modification.
Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 53 citations in OpenAlex.
- miR-501-5p mediates the progression of type 2 diabetic retinopathy by targeting NR2F2.Diabetology & metabolic syndrome · 2026Article
- Wound Healing: Molecular Mechanisms, Antimicrobial Peptides, and Emerging Technologies in Regenerative Medicine.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Glycosylation in kidney diseases.Precision clinical medicine · 2025Review
- Protein O-GlcNAcylation in reproductive biology and the impact of metabolic disease.Human reproduction update · 2025Review
- Divergent glucose stress responses in TM4 Sertoli cells: a miRNA-driven regulatory landscape of inflammation and cytokine expression.Molecular biology reports · 2025Article
- Pilot study on photoacoustic imaging and confocal Raman spectroscopy-derived biomarkers for assessing structural and physiological skin changes in atopic dermatitis and metabolic diseases.Biomedical optics express · 2025Article
- Glabridin Alleviates Oxidative Stress-Induced Osteoporosis by Targeting the Akt/NF-ĸB and Akt/GSK-3β Pathways.International journal of molecular sciences · 2025Article
- Interplay Between Metabolic Pathways and Increased Oxidative Stress in Human Red Blood Cells.Cells · 2024Review
- Unveiling the link between arsenic toxicity and diabetes: an in silico exploration into the role of transcription factors.Toxicological research · 2024Article
- Glycative stress as a cause of macular degeneration.Progress in retinal and eye research · 2024Review
- Diabetic Retinopathy: New Treatment Approaches Targeting Redox and Immune Mechanisms.Antioxidants (Basel, Switzerland) · 2024Review
- Correlation Between Glycemic Control and Serum Thyroglobulin Levels in a Patient With RAI-Refractory Thyroid Cancer.JCEM case reports · 2024Article
- Identifying transcriptomic profiles of iron-quercetin complex treated peripheral blood mononuclear cells from healthy volunteers and diabetic patients.Scientific reports · 2024Article
- Dynamics simulations of hypoxia inducible factor-1 regulatory network in cancer using formal verification techniques.Frontiers in molecular biosciences · 2024Article
- Risk Factors for Diabetic Retinopathy in Latin America (Mexico) and the World: A Systematic Review and Meta-Analysis.Journal of clinical medicine · 2023Article
- Association between diabetes and cancer. Current mechanistic insights into the association and future challenges.Molecular and cellular biochemistry · 2023Review
- Hyperglycemia and O-GlcNAc transferase activity drive a cancer stem cell pathway in triple-negative breast cancer.Cancer cell international · 2023Article
- Review
- Biological and Clinical Impacts of Glucose Metabolism in Pancreatic Ductal Adenocarcinoma.Cancers · 2023Review
- Spatiotemporal Proximity Labeling Tools to Track GlcNAc Sugar-Modified Functional Protein Hubs during Cellular Signaling.ACS chemical biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic hyperglycemia has been associated with an increased prevalence of pathological conditions including cardiovascular disease, cancer, or various disorders of the immune system. In some cases, these associations may be traced back to a common underlying cause, but more often, hyperglycemia and the disturbance in metabolic balance directly facilitate pathological changes in the regular cellular functions. One such cellular function crucial for every living organism is cell cycle regulation/mitotic activity. Although metabolic challenges have long been recognized to influence cell proliferation, the direct impact of diabetes on cell cycle regulatory elements is a relatively uncharted territory. Among other "nutrient sensing" mechanisms, protein O-linked β-N-acetylglucosamine (O-GlcNAc) modification emerged in recent years as a major contributor to the deleterious effects of hyperglycemia. An increasing amount of evidence suggest that O-GlcNAc may significantly influence the cell cycle and cellular proliferation. In our present review, we summarize the current data available on the direct impact of metabolic changes caused by hyperglycemia in pathological conditions associated with cell cycle disorders. We also review published experimental evidence supporting the hypothesis that O-GlcNAc modification may be one of the missing links between metabolic regulation and cellular proliferation.
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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.