Evidence map›Paper›PMID 28534084›Full record

ReviewCellular and molecular life sciences : CMLS2017

The emerging link between O-GlcNAcylation and neurological disorders.

Xiaofeng Ma, He Li, Yating He, Junwei Hao

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.9field-weighted citation impact, top 14% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Targeting O-GlcNAcylation in ischemic stroke.Neural regeneration research · 2022
    Article
  16. O-GlcNAcylation in Renal (Patho)Physiology.International journal of molecular sciences · 2022
    Review
  17. O-GlcNAcylation promotes cerebellum development and medulloblastoma oncogenesis via SHH signaling.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  18. Review
  19. Review
  20. O-GlcNAcylation in health and neurodegenerative diseases.Experimental & molecular medicine · 2021
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Xiaofeng MaDepartment of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
He LiDepartment of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Yating HeDepartment of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Junwei HaoDepartment of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China. hjw@tmu.edu.cn.
Tianjin Medical University General Hospital · CN

Funding

the National Natural Science Foundation of China 81273287the National Natural Science Foundation of China 81322018the National Natural Science Foundation of China 81401361the National Natural Science Foundation of China 81571600
6 · The paper itself

Abstract

O-linked β-N-acetylglucosaminylation (O-GlcNAcylation) is involved in the regulation of many cellular cascades and neurological diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and stroke. In the brain, the expression of O-GlcNAcylation is notably heightened, as is that of O-linked N-acetylglucosaminyltransferase (OGT) and β-N-acetylglucosaminidase (OGA), the presence of which is prominent in many regions of neurological importance. Most importantly, O-GlcNAcylation is believed to contribute to the normal functioning of neurons; conversely, its dysregulation participates in the pathogenesis of neurological disorders. In neurodegenerative diseases, O-GlcNAcylation of the brain's key proteins, such as tau and amyloid-β, interacts with their phosphorylation, thereby triggering the formation of neurofibrillary tangles and amyloid plaques. An increase of O-GlcNAcylation by pharmacological intervention prevents neuronal loss. Additionally, O-GlcNAcylation is stress sensitive, and its elevation is cytoprotective. Increased O-GlcNAcylation ameliorated brain damage in victims of both trauma-hemorrhage and stroke. In this review, we summarize the current understanding of O-GlcNAcylation's physiological and pathological roles in the nervous system and provide a foundation for development of a therapeutic strategy for neurological disorders.

Indexed as

Protein Processing, Post-TranslationalAcetylglucosamineAcetylglucosaminidaseAlzheimer DiseaseAmyotrophic Lateral SclerosisAnimalsBrainHumansN-AcetylglucosaminyltransferasesNervous System DiseasesNeuronsParkinson DiseaseProteinsAcetylglucosamineAcetylglucosaminidaseN-AcetylglucosaminyltransferasesProteinsAlzheimer’s diseaseAmyotrophic lateral sclerosisNeurological disordersO-GlcNAcylationParkinson’s diseaseStroke

Identifiers

PMID28534084
PMCPMC11107615
OpenAlexW2617826341

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.