ReviewCell communication and signaling : CCS2024
Role of O-linked N-acetylglucosamine protein modification in oxidative stress-induced autophagy: a novel target for bone remodeling.
Review in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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Who cites it
13 citing papers in PubMed.
- Rapid maxillary expansion related sutural and dentoalveolar changes provoke early-term oxidative stress.BMC oral health · 2026Trial
- Mechanical Unloading Inhibits Osteoblast Differentiation via Downregulation of OGT-Mediated O-GlcNAcylation.Current issues in molecular biology · 2026Article
- Multivariate genetic analysis reveals three distinct pathological dimensions in musculoskeletal disorders.Nature communications · 2026Article
- Research landscape, hotspots, and evolutionary trends of knee osteoarthritis and oxidative stress: a multidimensional bibliometric analysis.Frontiers in medicine · 2026Article
- Marine-Derived Quinolinone CHNQD-00603 Triggers Autophagy via Suppressing the AKT/ERK/mTOR Pathway to Reverse Senescence and Restore Osteogenic Potential in Bone Marrow Mesenchymal Stem Cells.Current protein & peptide science · 2026Article
- GLUL mediates FOXO3 O-GlcNAcylation to regulate the osteogenic differentiation of BMSCs and senile osteoporosis.Cell death and differentiation · 2025Article
- Active Inclusion Bodies in the Multienzymatic Synthesis of UDP-N-acetylglucosamine.International journal of molecular sciences · 2025Article
- O‑GlcNAcylation: The crosstalk between infection immunity and autophagy in sepsis (Review).Molecular medicine reports · 2025Review
- IRS2/FOXO1 mitigates osteoarthritis by regulating chondrocyte autophagy and mitochondrial function.Molecular medicine (Cambridge, Mass.) · 2025Article
- The dual-coding gene SLC35A4 protects against oxidative stress.Protein science : a publication of the Protein Society · 2025Article
- Binary curcuminoid complex CRE-Bin inhibits osteoclast differentiation by suppressing the canonical NF-κB signaling pathway and modulating microRNA-223 expression.Scientific reports · 2025Article
- Potential threats of environmental microplastics to the skeletal system: current insights and future directions.Frontiers in endocrinology · 2025Review
- Application of autophagy in mesenchymal stem cells.World journal of stem cells · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
O-linked N-acetylglucosamine protein modification (O-GlcNAcylation) is a dynamic post-translational modification (PTM) involving the covalent binding of serine and/or threonine residues, which regulates bone cell homeostasis. Reactive oxygen species (ROS) are increased due to oxidative stress in various pathological contexts related to bone remodeling, such as osteoporosis, arthritis, and bone fracture. Autophagy serves as a scavenger for ROS within bone marrow-derived mesenchymal stem cells, osteoclasts, and osteoblasts. However, oxidative stress-induced autophagy is affected by the metabolic status, leading to unfavorable clinical outcomes. O-GlcNAcylation can regulate the autophagy process both directly and indirectly through oxidative stress-related signaling pathways, ultimately improving bone remodeling. The present interventions for the bone remodeling process often focus on promoting osteogenesis or inhibiting osteoclast absorption, ignoring the effect of PTM on the overall process of bone remodeling. This review explores how O-GlcNAcylation synergizes with autophagy to exert multiple regulatory effects on bone remodeling under oxidative stress stimulation, indicating the application of O-GlcNAcylation as a new molecular target in the field of bone remodeling.
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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.