ReviewMedComm2025
Protein O-GlcNAcylation in Health and Diseases.
Review in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Mechanical Unloading Inhibits Osteoblast Differentiation via Downregulation of OGT-Mediated O-GlcNAcylation.Current issues in molecular biology · 2026Article
- TGFBI Maintains Fibrocartilage Homeostasis by Restraining O-GlcNAcylation to Inactivate and Destabilize ADAMTS16 in Temporomandibular Joint Osteoarthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cross-talk between glycosylation pathways: Mechanistic insights and implications for human diseases.Molecular metabolism · 2026Review
- Myokine Cathepsin B as a Key Muscle-Brain Axis Regulator Mediates Treadmill-Running-Induced Hippocampal Neurogenesis and Cognitive Improvement in Mice.Research (Washington, D.C.) · 2026Article
- Protein O-GlcNAcylation in Health and Diseases.MedComm · 2025Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
O-GlcNAcylation is a reversible posttranslational modification of proteins that has garnered significant attention in recent years. By regulating the structure and function of proteins, it plays a critical role in various biological processes. Normal O-GlcNAcylation is essential for maintaining internal homeostasis and is involved in controlling fundamental biological events such as gene expression, the cell cycle regulation, metabolism, and signal transduction. Conversely, aberrant O-GlcNAcylation is closely linked to the onset and progression of various diseases-including neurodegenerative diseases, cancers, cardiovascular diseases, and immune-related diseases-where it drives pathological development. Currently, there is a lack of comprehensive reviews systematically addressing the specific mechanisms of O-GlcNAcylation under both physiological and pathological conditions. Therefore, this article aims to summarize its dual role in maintaining organismal homeostasis and promoting disease pathogenesis, providing an integrated evaluation of the biological significance of this modification in health and diseases. Furthermore, it discusses the potential of O-GlcNAcylation as a therapeutic target, explores its clinical applications, and analyzes the current challenges and future directions in drug development, thereby offering theoretical insights and research perspectives for related fields.
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.