Evidence map›Paper›PMID 29323156›Full record

ArticleScientific reports2018

Ischemia-induced Neuronal Cell Death Is Mediated by Chemokine Receptor CX3CR1.

Jinkun Wang, Yan Gan, Pengcheng Han, Junxiang Yin, Qingwei Liu, Soha Ghanian, Feng Gao, Guanghui Gong, Zhiwei Tang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.3field-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

39 citing papers in PubMed, 54 citations in OpenAlex.

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  5. TNF-α Inhibition Modulates CX3CR1, Pyroptosis-related Genes, and BDNF to Alleviate Anxiety-like Behavior in Type 2 Diabetic Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
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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

9 authors at 4 institutions in 2 countries.

Jinkun WangDepartment of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Yan GanDepartment of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Pengcheng HanDepartment of Neurology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ, USA.
Junxiang YinDepartment of Neurology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ, USA.
Qingwei LiuDepartment of Radiology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ, USA.
Soha GhanianDepartment of Neurology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ, USA.
Feng GaoDepartment of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Guanghui GongDepartment of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Zhiwei TangDepartment of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China. tangzhiwei7755@hotmail.com.
Barrow Neurological Institute · USSt. Joseph's Hospital and Medical Center · USFirst Affiliated Hospital of Kunming Medical University · CNKunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The chemokine fractalkine (CX3CL1) and its receptor CX3CR1 play a fundamental role in the pathophysiology of stroke. Previous studies have focused on a paracrine interaction between neurons that produce fractalkine and microglia that express CX3CR1 receptors in the central nervous system. Recent findings have demonstrated the functional expression of CX3CR1 receptors by hippocampal neurons, suggesting their involvement in neuroprotective and neurodegenerative actions. To elucidate the roles of neuronal CX3CR1 in neurodegeneration induced by ischemic stroke, a mouse model of permanent middle cerebral artery occlusion (pMCAO) was employed. In the pMCAO mice, increased CX3CR1 levels, apoptosis-associated morphological changes, and Caspase 3-positive neuronal cells were observed in the striatum and in the hippocampus 24 hours after occlusion. Upregulation of CX3CR1 in ischemic neurons is associated with neuronal apoptotic cell death. In contrast, ischemia-induced apoptotic neuronal cell death was decreased in CX3CR1 deficient mice. Cultured primary hippocampal neurons obtained from CX3CR1 deficient mice were more resistant to glutamate-induced excitotoxicity by blocking calcium influx than those from wild-type mice. For the first time, we reported that neuronal CXCR1 mediates neuronal apoptotic cell death in ischemia. Our results suggest that modulating CXCR1 activity offers a novel therapeutic strategy for stroke.

Indexed as

ApoptosisAnimalsCalciumCells, CulturedCorpus StriatumCX3C Chemokine Receptor 1Glutamic AcidHippocampusInfarction, Middle Cerebral ArteryMaleMiceMice, Inbred C57BLNeuronsUp-RegulationCalciumCX3C Chemokine Receptor 1Cx3cr1 protein, mouseGlutamic Acid

Identifiers

PMID29323156
PMCPMC5765008
OpenAlexW2782347637

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.