Evidence map›Paper›PMID 28264978›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017

Deletion of the Fractalkine Receptor, CX3CR1, Improves Endogenous Repair, Axon Sprouting, and Synaptogenesis after Spinal Cord Injury in Mice.

Camila M Freria, Jodie C E Hall, Ping Wei, Zhen Guan, Dana M McTigue, Phillip G Popovich

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
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  16. Synapse Regulation.Advances in neurobiology · 2024
    Review
  17. Article
  18. CSF IL-8 Associated with Response to Gene Therapy in a Case Series of Spinal Muscular Atrophy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
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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.

Camila M FreriaDepartment of Neuroscience and Center for Brain and Spinal Cord Repair, Ohio State University, Wexner Medical Center, Columbus, Ohio 43210.ORCID 0000-0002-3171-8141
Jodie C E HallDepartment of Neuroscience and Center for Brain and Spinal Cord Repair, Ohio State University, Wexner Medical Center, Columbus, Ohio 43210.ORCID 0000-0002-4820-6070
Ping WeiDepartment of Neuroscience and Center for Brain and Spinal Cord Repair, Ohio State University, Wexner Medical Center, Columbus, Ohio 43210.
Zhen GuanDepartment of Neuroscience and Center for Brain and Spinal Cord Repair, Ohio State University, Wexner Medical Center, Columbus, Ohio 43210.
Dana M McTigueDepartment of Neuroscience and Center for Brain and Spinal Cord Repair, Ohio State University, Wexner Medical Center, Columbus, Ohio 43210.ORCID 0000-0001-7066-9701
Phillip G PopovichDepartment of Neuroscience and Center for Brain and Spinal Cord Repair, Ohio State University, Wexner Medical Center, Columbus, Ohio 43210 phillip.popovich@osumc.edu.ORCID 0000-0003-1329-7395
The Ohio State University Wexner Medical Center · US

Funding

Preventing autonomic dysreflexia to restore immune function after SCIR01NS083942 · NINDS · OHIO STATE UNIVERSITY · PI POPOVICH, PHILLIP G · 2014 to 2018
$2.2M
NINDS NIH HHS R01 NS083942
6 · The paper itself

Abstract

Impaired signaling via CX3CR1, the fractalkine receptor, promotes recovery after traumatic spinal contusion injury in mice, a benefit achieved in part by reducing macrophage-mediated injury at the lesion epicenter. Here, we tested the hypothesis that CX3CR1-dependent changes in microglia and macrophage functions also will enhance neuroplasticity, at and several segments below the injury epicenter. New data show that in the presence of inflammatory stimuli, CX3CR1-deficient (CX3CR1

Indexed as

AnimalsCX3C Chemokine Receptor 1FemaleGene DeletionGenetic TherapyMaleMiceMice, Inbred C57BLNeuronal OutgrowthReceptors, ChemokineSpinal Cord InjuriesSpinal Cord RegenerationSynapsesTreatment OutcomeCX3C Chemokine Receptor 1Cx3cr1 protein, mouseReceptors, ChemokineCX3CR1inflammationmacrophagesmicrogliaplasticityspinal cord injury

Identifiers

PMID28264978
PMCPMC5373135
OpenAlexW2594903711

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.