Evidence map›Paper›PMID 33682795›Full record

ArticleJCI insight2021

Inhibition of astrocyte hemichannel improves recovery from spinal cord injury.

Chao Zhang, Zhao Yan, Asif Maknojia, Manuel A Riquelme, Sumin Gu, Grant Booher, David J Wallace, Viktor Bartanusz, Akshay Goswami, Wei Xiong and 5 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Role of astrocytes connexins - pannexins in acute brain injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Evaluation of Connexin Hemichannel Activity In Vivo.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  15. Hemichannels contribute to mitochondrial CaFrontiers in cell and developmental biology · 2024
    Article
  16. 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

15 authors at 4 institutions in 2 countries.

Chao ZhangDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
Zhao YanDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
Asif MaknojiaDepartment of Neurosurgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
Manuel A RiquelmeDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
Sumin GuDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
Grant BooherDepartment of Neurosurgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
David J WallaceDepartment of Neurosurgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
Viktor BartanuszDepartment of Neurosurgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
Akshay GoswamiDepartment of Neurosurgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
Wei XiongTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Ningyan ZhangTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Michael J MaderAudie L. Murphy VA Hospital, South Texas Veteran's Health Care System, San Antonio, Texas, USA.
Zhiqiang AnTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Naomi L SayreDepartment of Neurosurgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
Jean X JiangDepartment of Biochemistry and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
The University of Texas Health Science Center at San Antonio · USBrown Foundation · USCentral South University · CNAudie L. Murphy Memorial VA Hospital · US

Funding

Connexin channels in transducing mechanical signals in boneR01AR072020 · NIAMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JIANG, JEAN X · 2018 to 2022
$1.7M
NIAMS NIH HHS R01 AR072020
6 · The paper itself

Abstract

Spinal cord injury (SCI) causes severe disability, and the current inability to restore function to the damaged spinal cord leads to lasting detrimental consequences to patients. One strategy to reduce SCI morbidity involves limiting the spread of secondary damage after injury. Previous studies have shown that connexin 43 (Cx43), a gap junction protein richly expressed in spinal cord astrocytes, is a potential mediator of secondary damage. Here, we developed a specific inhibitory antibody, mouse-human chimeric MHC1 antibody (MHC1), that inhibited Cx43 hemichannels, but not gap junctions, and reduced secondary damage in 2 incomplete SCI mouse models. MHC1 inhibited the activation of Cx43 hemichannels in both primary spinal astrocytes and astrocytes in situ. In both SCI mouse models, administration of MHC1 after SCI significantly improved hind limb locomotion function. Remarkably, a single administration of MHC1 30 minutes after injury improved the recovery up to 8 weeks post-SCI. Moreover, MHC1 treatment decreased gliosis and lesion sizes, increased white and gray matter sparing, and improved neuronal survival. Together, these results suggest that inhibition of Cx43 hemichannel function after traumatic SCI reduces secondary damage, limits perilesional gliosis, and improves functional recovery. By targeting hemichannels specifically with an antibody, this study provides a potentially new, innovative therapeutic approach in treating SCI.

Indexed as

Recovery of FunctionAnimalsAntibodies, MonoclonalAstrocytesConnexin 43ConnexinsDisease Models, AnimalGliosisHumansLocomotionMaleMiceMice, Inbred C57BLMotor ActivityNeuroprotective AgentsSpinal CordAntibodies, MonoclonalConnexin 43ConnexinsGJA1 protein, humanNeuroprotective AgentsNeurological disordersTherapeutics

Identifiers

PMID33682795
PMCPMC8021110
OpenAlexW3135672754

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.