Evidence map›Paper›PMID 39327578›Full record

ArticleCell communication and signaling : CCS2024

Fractalkine/CX3CR1 axis is critical for neuroprotection induced by hypoxic postconditioning against cerebral ischemic injury.

Lixuan Zhan, Meiqian Qiu, Jianhua Zheng, Meijing Lai, Kunqin Lin, Jiahua Dai, Weiwen Sun, En Xu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

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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

9 citing papers in PubMed.

  1. Review
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  4. Article
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  6. Synthetic Cyclic CAntioxidants (Basel, Switzerland) · 2025
    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

8 authors.

Lixuan Zhan *Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China.
Meiqian Qiu *Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China.
Jianhua ZhengDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China.
Meijing LaiDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China.
Kunqin LinDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China.
Jiahua DaiDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China.
Weiwen SunDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China.
En XuDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, 250 Changgang Dong RD, Guangzhou, 510260, P. R. China. enxu@163.net.

Funding

Key Medical Disciplines and Specialties Program of Guangzhou 2021-2023National Natural Science Foundation of China No. 82071281National Natural Science Foundation of China No. 82271330Natural Science Foundation of Guangdong Province No. 2021A1515011269
6 · The paper itself

Abstract

Microglial activation-mediated neuroinflammation is a major contributor to neuronal damage after cerebral ischemia. The Fractalkine (FKN)/CX3C chemokine receptor 1 (CX3CR1) axis plays a critical role in regulating microglial activation and neuroinflammation. The aim of this study is to ascertain the role and mechanism of FKN/CX3CR1 axis in hypoxic postconditioning (HPC)-induced anti-inflammatory and neuroprotective effects on transient global cerebral ischemia (tGCI). We found that HPC suppressed microglial activation and alleviated neuroinflammation in hippocampal CA1 after tGCI. Meanwhile, HPC upregulated the expression of FKN and CX3CR1 in neurons, but it downregulated the expression of CX3CR1 in glial cells after tGCI. In addition, the overexpression of FKN induced by the administration of FKN-carried lentivirus reduced microglial activation and inhibited neuroinflammation in CA1 after tGCI. Furthermore, silencing CX3CR1 with CX3CRi-carried lentivirus in CA1 after tGCI suppressed microglial activation and neuroinflammation and exerted neuroprotective effects. Finally, the overexpression of FKN caused a marked increase of neuronal CX3CR1 receptors, upregulated the phosphorylation of Akt, and reduced neuronal loss of rats in CA1 after tGCI. These findings demonstrated that HPC protected against neuronal damage in CA1 of tGCI rats through inhibiting microglial activation and activating Akt signaling pathway via FKN/CX3CR1 axis.

Indexed as

Chemokine CX3CL1CX3C Chemokine Receptor 1MicrogliaNeuroprotectionAnimalsBrain IschemiaCA1 Region, HippocampalIschemic PostconditioningMaleNeuronsRatsRats, Sprague-DawleySignal TransductionChemokine CX3CL1CX3C Chemokine Receptor 1CX3CR1 protein, ratAktCerebral ischemiaCX3CR1FractalkineHypoxic postconditioningNeuroinflammation

Identifiers

PMID39327578
PMCPMC11426015

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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.