ReviewFree radical research2016
The regulatory roles of O-GlcNAcylation in mitochondrial homeostasis and metabolic syndrome.
Review in Free radical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis 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
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- The human O-GlcNAcome database and meta-analysis.Scientific data · 2021Pooled it
- Alcohol Reprograms Placental Glucose and Lipid Metabolism, Which Correlate with Reduced Fetal Brain but not Body Weight in a Mouse Model of Prenatal Alcohol Exposure.The Journal of nutrition · 2025Article
- O-GlcNAc participates in the meiosis of aging oocytes by mediating mitochondrial function.Reproduction (Cambridge, England) · 2024Article
- Identification of a Polypeptide Inhibitor ofJournal of the American Chemical Society · 2024Article
- Roles of O-GlcNAcylation in Mitochondrial Homeostasis and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Protective effect of increased O-GlcNAc cycling against 6-OHDA induced Parkinson's disease pathology.Cell death & disease · 2024Article
- The Role of Astrocytic Mitochondria in the Pathogenesis of Brain Ischemia.Molecular neurobiology · 2024Review
- Low glucose induced Alzheimer's disease-like biochemical changes in human induced pluripotent stem cell-derived neurons is due to dysregulated O-GlcNAcylation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Altered O-GlcNAcylation and mitochondrial dysfunction, a molecular link between brain glucose dysregulation and sporadic Alzheimer's disease.Neural regeneration research · 2023Article
- Chemical Biology Approaches to Understanding Neuronal O-GlcNAcylation.Israel journal of chemistry · 2023Article
- Review
- ProteinMetabolites · 2022Review
- Spatial and temporal proteomics reveals the distinct distributions and dynamics of O-GlcNAcylated proteins.Cell reports · 2022Article
- The intra-mitochondrial O-GlcNAcylation system rapidly modulates OXPHOS function and ROS release in the heart.Communications biology · 2022Article
- Current Challenges of Mitochondrial Potassium Channel Research.Frontiers in physiology · 2022Review
- OGT Regulates Mitochondrial Biogenesis and Function via Diabetes Susceptibility Gene Pdx1.Diabetes · 2021Article
- Effects of O-GlcNAcylation on functional mitochondrial transfer from astrocytes.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- ExcessiveCirculation · 2021Article
- High-Fat Diet Leads to Reduced Protein O-GlcNAcylation and Mitochondrial Defects Promoting the Development of Alzheimer's Disease Signatures.International journal of molecular sciences · 2021Article
- Central and Peripheral Metabolic Defects Contribute to the Pathogenesis of Alzheimer's Disease: Targeting Mitochondria for Diagnosis and Prevention.Antioxidants & redox signaling · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Nutrients excess is one of the leading causes of metabolic syndrome globally. Protein post-translational O-GlcNAc modification has been recognized as an essential nutrient sensor of the cell. Emerging studies suggest that O-GlcNAcylation lies at the core linking nutritional stress to insulin resistance. Mitochondria are the major site for ATP production in most eukaryotes. Mitochondrial dysfunction and oxidative stress have long been considered as an important mechanism underlying insulin resistance. The metabolic process is under the influence of environmental and nutritional factors, thus sensing and transducing nutritional signals sit at the pivot of metabolism control. For a long time little was known about O-GlcNAcylation within mitochondria since mitochondrial O-GlcNAcylation was regarded rare. Recent findings have demonstrated that O-GlcNAcylation is widely spread among mitochondrial proteins, and that mitochondrial function and oxidative stress both can be regulated by O-GlcNAcylation, particularly under diabetic circumstances.
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.