Evidence map›Paper›PMID 39940727›Full record

ReviewInternational journal of molecular sciences2025

CX3CL1 Regulation of Gliosis in Neuroinflammatory and Neuroprotective Processes.

Irene L Gutiérrez, David Martín-Hernández, Karina S MacDowell, Borja García-Bueno, Javier R Caso, Juan C Leza, José L M Madrigal

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

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

12 citing papers in PubMed.

  1. Article
  2. Single-Cell Profiling Reveals Clonally Expanded CX3CR1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

7 authors.

Irene L GutiérrezDepartment of Pharmacology and Toxicology, School of Medicine, Universidad Complutense de Madrid (UCM), Av. Complutense s/n, 28040, Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Instituto de Investigación Neuroquímica (IUINQ-UCM), Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12), 28040 Madrid, Spain.
David Martín-HernándezDepartment of Pharmacology and Toxicology, School of Medicine, Universidad Complutense de Madrid (UCM), Av. Complutense s/n, 28040, Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Instituto de Investigación Neuroquímica (IUINQ-UCM), Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12), 28040 Madrid, Spain.ORCID 0000-0003-0195-2604
Karina S MacDowellDepartment of Pharmacology and Toxicology, School of Medicine, Universidad Complutense de Madrid (UCM), Av. Complutense s/n, 28040, Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Instituto de Investigación Neuroquímica (IUINQ-UCM), Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12), 28040 Madrid, Spain.ORCID 0000-0002-1527-8895
Borja García-BuenoDepartment of Pharmacology and Toxicology, School of Medicine, Universidad Complutense de Madrid (UCM), Av. Complutense s/n, 28040, Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Instituto de Investigación Neuroquímica (IUINQ-UCM), Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12), 28040 Madrid, Spain.
Javier R CasoDepartment of Pharmacology and Toxicology, School of Medicine, Universidad Complutense de Madrid (UCM), Av. Complutense s/n, 28040, Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Instituto de Investigación Neuroquímica (IUINQ-UCM), Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12), 28040 Madrid, Spain.ORCID 0000-0001-8622-749X
Juan C LezaDepartment of Pharmacology and Toxicology, School of Medicine, Universidad Complutense de Madrid (UCM), Av. Complutense s/n, 28040, Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Instituto de Investigación Neuroquímica (IUINQ-UCM), Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12), 28040 Madrid, Spain.
José L M MadrigalDepartment of Pharmacology and Toxicology, School of Medicine, Universidad Complutense de Madrid (UCM), Av. Complutense s/n, 28040, Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Instituto de Investigación Neuroquímica (IUINQ-UCM), Instituto de Investigación Sanitaria Hospital 12 de Octubre (Imas12), 28040 Madrid, Spain.ORCID 0000-0002-1409-9561

Funding

Ministerio de Ciencia, Innovación y Universidades PID2021-123871OB-I00
6 · The paper itself

Abstract

Among the different chemokines, C-X3-C motif chemokine ligand 1 or CX3CL1, also named fractalkine, is one of the most interesting due to its characteristics, including its unique structure, not shared by any other chemokine, and its ability to function both in a membrane-bound form and in a soluble form, among others. However, undoubtedly, its most relevant characteristic from the neuroscientific point of view is its role as a messenger used by neurons to communicate with microglia. The study of the interaction between both cell types and the key role that CX3CL1 seems to play has facilitated the identification of CX3CL1 as a crucial modulator of microglial activation and a promising target in the fight against neuroinflammation. As a result, numerous studies have contributed to elucidate the involvement of CX3CL1 and its specific receptor CCX3CR1 in the progression of different neuroinflammatory and neurodegenerative processes, with Alzheimer's and Parkinson's diseases being the most studied ones. However, the different animal and cellular models used to reproduce the pathological conditions to be analyzed, as well as the difficulties inherent to studies performed on human samples, have hindered the collection of compatible results in many cases. In this review, we summarize some of the most relevant data describing the alterations found for the CX3CL1/CX3CR1 signaling axis in different neurodegenerative conditions in which neuroinflammation is known to play a relevant role.

Indexed as

Chemokine CX3CL1GliosisNeuroinflammatory DiseasesNeuroprotectionAnimalsCX3C Chemokine Receptor 1HumansMicrogliaNeurodegenerative DiseasesSignal TransductionChemokine CX3CL1CX3C Chemokine Receptor 1CX3CL1 protein, humanchemokinesCX3CL1CX3CR1fractalkinemicroglianeurodegenerationneuroinflammationneurons

Identifiers

PMID39940727
PMCPMC11817243

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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.