Evidence map›Paper›PMID 32116564›Full record

ReviewFrontiers in cellular neuroscience2020

Metabolic Regulation of Glial Phenotypes: Implications in Neuron-Glia Interactions and Neurological Disorders.

Ruqayya Afridi, Jong-Heon Kim, Md Habibur Rahman, Kyoungho Suk

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07364162 (Exogenous Ketone Ester Supplementation in ICU Delirium), which is not on this map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
5.8field-weighted citation impact, top 3% 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.

NCT07364162 phase2recruitingnot on this mapstarted 2026, after this paper: background citation

Exogenous Ketone Ester Supplementation in ICU Delirium (KETONES ICU)

TypeinterventionalSponsorVanderbilt University Medical CenterRan2026 to 2027Enrolled40ConditionsICU Delirium, Critical IllnessArmsKetone monoester, Placebo
3 · Its place in the literature

Who cites it

62 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Regulation of Metabolic Rhythms by Glial Clocks.Journal of biological rhythms · 2026
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Astrocytic EphA4 signaling is important for the elimination of excitatory synapses in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review

2 more citing papers are in PubMed but not listed here.

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.

Ruqayya AfridiBK21 Plus KNU Biomedical Convergence Program, Department of Pharmacology, Brain Science and Engineering Institute, School of Medicine, Kyungpook National University, Daegu, South Korea.
Jong-Heon KimBK21 Plus KNU Biomedical Convergence Program, Department of Pharmacology, Brain Science and Engineering Institute, School of Medicine, Kyungpook National University, Daegu, South Korea.
Md Habibur RahmanBK21 Plus KNU Biomedical Convergence Program, Department of Pharmacology, Brain Science and Engineering Institute, School of Medicine, Kyungpook National University, Daegu, South Korea.
Kyoungho SukBK21 Plus KNU Biomedical Convergence Program, Department of Pharmacology, Brain Science and Engineering Institute, School of Medicine, Kyungpook National University, Daegu, South Korea.
Kyungpook National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glial cells are multifunctional, non-neuronal components of the central nervous system with diverse phenotypes that have gained much attention for their close involvement in neuroinflammation and neurodegenerative diseases. Glial phenotypes are primarily characterized by their structural and functional changes in response to various stimuli, which can be either neuroprotective or neurotoxic. The reliance of neurons on glial cells is essential to fulfill the energy demands of the brain for its proper functioning. Moreover, the glial cells perform distinct functions to regulate their own metabolic activities, as well as work in close conjunction with neurons through various secreted signaling or guidance molecules, thereby constituting a complex network of neuron-glial interactions in health and disease. The emerging evidence suggests that, in disease conditions, the metabolic alterations in the glial cells can induce structural and functional changes together with neuronal dysfunction indicating the importance of neuron-glia interactions in the pathophysiology of neurological disorders. This review covers the recent developments that implicate the regulation of glial phenotypic changes and its consequences on neuron-glia interactions in neurological disorders. Finally, we discuss the possibilities and challenges of targeting glial metabolism as a strategy to treat neurological disorders.

Indexed as

gliametabolismneurological disordersneuronneuron–glia interaction

Identifiers

PMID32116564
PMCPMC7026370
OpenAlexW3005708093

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.