Evidence map›Paper›PMID 32849190›Full record

ReviewFrontiers in neurology2020

The Multifaceted Role of Astrocyte Connexin 43 in Ischemic Stroke Through Forming Hemichannels and Gap Junctions.

Zhen Liang, Xu Wang, Yulei Hao, Lin Qiu, Yingyue Lou, Yaoting Zhang, Di Ma, Jiachun Feng

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 5% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Channels and Transporters in Ischemic Brain Edema.Journal of inflammation research · 2025
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Mechanobiological Modulation ofACS biomaterials science & engineering · 2024
    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

8 authors at 2 institutions in 1 country.

Zhen LiangDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
Xu WangDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
Yulei HaoDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
Lin QiuDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
Yingyue LouDepartment of Plastic and Reconstructive Surgery, The First Hospital of Jilin University, Changchun, China.
Yaoting ZhangDepartment of Cardiology, The First Hospital of Jilin University, Changchun, China.
Di MaDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
Jiachun FengDepartment of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
First Hospital of Jilin University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic stroke is a multi-factorial cerebrovascular disease with high worldwide morbidity and mortality. In the past few years, multiple studies have revealed the underlying mechanism of ischemia/reperfusion injury, including calcium overload, amino acid toxicity, oxidative stress, and inflammation. Connexin 43 (Cx43), the predominant connexin protein in astrocytes, has been recently proven to display non-substitutable roles in the pathology of ischemic stroke development and progression through forming gap junctions and hemichannels. Under normal conditions, astrocytic Cx43 could be found in hemichannels or in the coupling with other hemichannels on astrocytes, neurons, or oligodendrocytes to form the neuro-glial syncytium, which is involved in metabolites exchange between communicated cells, thus maintaining the homeostasis of the CNS environment. In ischemic stroke, the phosphorylation of Cx43 might cause the degradation of gap junctions and the opening of hemichannels, contributing to the release of inflammatory mediators. However, the remaining gap junctions could facilitate the exchange of protective and harmful metabolites between healthy and injured cells, protecting the injured cells to some extent or damaging the healthy cells depending on the balance of the exchange of protective and harmful metabolites. In this study, we review the changes in astrocytic Cx43 expression and distribution as well as the influence of these changes on the function of astrocytes and other cells in the CNS, providing new insight into the pathology of ischemic stroke injury; we also discuss the potential of astrocytic Cx43 as a target for the treatment of ischemic stroke.

Indexed as

astrocyteconnexin 43gap junctionhemichannelischemic strokesyncytium

Identifiers

PMID32849190
PMCPMC7411525
OpenAlexW3046832479

What Socratic 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 Socratic graph.