Evidence map›Paper›PMID 32244528›Full record

ReviewCells2020

Role of Connexins 30, 36, and 43 in Brain Tumors, Neurodegenerative Diseases, and Neuroprotection.

Oscar F Sánchez, Andrea V Rodríguez, José M Velasco-España, Laura C Murillo, Jhon-Jairo Sutachan, Sonia-Luz Albarracin

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Connexin-Pannexin duality in glioblastoma.Cell and tissue research · 2026
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Ion Channels in Gliomas-From Molecular Basis to Treatment.International journal of molecular sciences · 2023
    Review
  17. Article
  18. Review
  19. Article
  20. Article
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

6 authors at 1 institution in 1 country.

Oscar F SánchezDepartment of Nutrition and Biochemistry, Pontificia Universidad Javeriana, 110911 Bogota, Colombia.ORCID 0000-0003-2237-0945
Andrea V RodríguezDepartment of Nutrition and Biochemistry, Pontificia Universidad Javeriana, 110911 Bogota, Colombia.
José M Velasco-EspañaDepartment of Nutrition and Biochemistry, Pontificia Universidad Javeriana, 110911 Bogota, Colombia.
Laura C MurilloDepartment of Nutrition and Biochemistry, Pontificia Universidad Javeriana, 110911 Bogota, Colombia.ORCID 0000-0002-3148-5982
Jhon-Jairo SutachanDepartment of Nutrition and Biochemistry, Pontificia Universidad Javeriana, 110911 Bogota, Colombia.
Sonia-Luz AlbarracinDepartment of Nutrition and Biochemistry, Pontificia Universidad Javeriana, 110911 Bogota, Colombia.
Pontificia Universidad Javeriana · CO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gap junction (GJ) channels and their connexins (Cxs) are complex proteins that have essential functions in cell communication processes in the central nervous system (CNS). Neurons, astrocytes, oligodendrocytes, and microglial cells express an extraordinary repertory of Cxs that are important for cell to cell communication and diffusion of metabolites, ions, neurotransmitters, and gliotransmitters. GJs and Cxs not only contribute to the normal function of the CNS but also the pathological progress of several diseases, such as cancer and neurodegenerative diseases. Besides, they have important roles in mediating neuroprotection by internal or external molecules. However, regulation of Cx expression by epigenetic mechanisms has not been fully elucidated. In this review, we provide an overview of the known mechanisms that regulate the expression of the most abundant Cxs in the central nervous system, Cx30, Cx36, and Cx43, and their role in brain cancer, CNS disorders, and neuroprotection. Initially, we focus on describing the Cx gene structure and how this is regulated by epigenetic mechanisms. Then, the posttranslational modifications that mediate the activity and stability of Cxs are reviewed. Finally, the role of GJs and Cxs in glioblastoma, Alzheimer's, Parkinson's, and Huntington's diseases, and neuroprotection are analyzed with the aim of shedding light in the possibility of using Cx regulators as potential therapeutic molecules.

Indexed as

NeuroprotectionAnimalsBrain NeoplasmsCentral Nervous SystemConnexinsEpigenesis, GeneticHumansNeurodegenerative DiseasesProtein Processing, Post-TranslationalConnexinsastrocytesconnexinsepigeneticsgap junctionsmicroglianeurodegenerative diseasesneuronsneuroprotection

Identifiers

PMID32244528
PMCPMC7226843
OpenAlexW3014227566

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.