ReviewMolecular neurobiology2017
Analysis of the Role of CX3CL1 (Fractalkine) and Its Receptor CX3CR1 in Traumatic Brain and Spinal Cord Injury: Insight into Recent Advances in Actions of Neurochemokine Agents.
Review in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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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.
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.
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Who cites it
60 citing papers in PubMed, 101 citations in OpenAlex.
- Utility of selected neuroinflammatory markers following lethal traumatic brain injury: a combined biofluid and tissue-based assessment of TNF-α, CX3CL1, TNFR1, TNFR2 and CX3CR1 expression.International journal of legal medicine · 2026Article
- Antidepressant-like effects of ketamine involve CXTranslational psychiatry · 2026Article
- Integrative bulk and single-cell transcriptome analyses reveal RNA modification-related biomarkers of spinal cord injury.Neural regeneration research · 2026Article
- Endothelin-1 induces Zfp36 family RNA-binding proteins and restrains cytokine and chemokine production in reactive astrocytes.The Journal of biological chemistry · 2026Article
- The ADAM Family of Proteases: Structure, Substrates, and Roles in Liver Diseases.International journal of molecular sciences · 2026Review
- Fractalkine (Chemokine CX3CL1) Signaling During Placentation and Placental Function.International journal of molecular sciences · 2026Review
- Progress on Omega-3 fatty acids for the comprehensive and targeted treatment of spinal cord injury.Bone research · 2026Review
- Glycosaminoglycan binding to soluble CX3CL1 impacts monocyte migrationFrontiers in immunology · 2026Article
- Special Issue "Fractalkine (CX3CL1) and Its Chemoattractant and Adhesion Molecule Properties in Health and Disease".International journal of molecular sciences · 2025Article
- Human induced pluripotent stem cell-derived microglia with a CX3CR1-V249I genetic variant exhibit dysfunctional phenotypes and modulate neuronal growth and function.bioRxiv : the preprint server for biology · 2025Article
- Centripetal migration and prolonged retention of microglia promotes spinal cord injury repair.Journal of neuroinflammation · 2025Article
- Microglia-orchestrated neuroinflammation and synaptic remodeling: roles of pro-inflammatory cytokines and receptors in neurodegeneration.Frontiers in cellular neuroscience · 2025Review
- Decoding the genetic landscape of autism: A comprehensive review.World journal of clinical pediatrics · 2024Article
- CX3CL1 (Fractalkine)-CX3CR1 Axis in Inflammation-Induced Angiogenesis and Tumorigenesis.International journal of molecular sciences · 2024Review
- Alterations in CX3CL1 Levels and Its Role in Viral Pathogenesis.International journal of molecular sciences · 2024Review
- CX3CL1/CX3CR1 Signaling Mediated Neuroglia Activation Is Implicated in the Retinal Degeneration: A Potential Therapeutic Target to Prevent Photoreceptor Death.Investigative ophthalmology & visual science · 2024Article
- Silymarin administration after cerebral ischemia improves survival of obese mice by increasing cortical BDNF and IGF1 levels.Frontiers in aging neuroscience · 2024Article
- Alpha-1 antitrypsin inhibits fractalkine-mediated monocyte-lung endothelial cell interactions.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Neuromuscular defects after infection with a beta coronavirus in mice.Neurochemistry international · 2023Article
- Microglial transglutaminase 2 deficiency causes impaired synaptic remodelling and cognitive deficits in mice.Cell proliferation · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CX3CL1 (fractalkine) is the only member of the CX3C (delta) subfamily of chemokines which is unique and combines the properties of both chemoattractant and adhesion molecules. The two-form ligand can exist either in a soluble form, like all other chemokines, and as a membrane-anchored molecule. CX3CL1 discloses its biological properties through interaction with one dedicated CX3CR1 receptor which belongs to a family of G protein-coupled receptors (GPCR). The CX3CL1/CX3CR1 axis acts in many physiological phenomena including those occurring in the central nervous system (CNS), by regulating the interactions between neurons, microglia, and immune cells. Apart from the role under physiological conditions, the CX3CL1/CX3CR1 axis was implied to have a role in different neuropathologies such as traumatic brain injury (TBI) and spinal cord injury (SCI). CNS injuries represent a serious public health problem, despite improvements in therapeutic management. To date, no effective treatment has been determined, so they constitute a leading cause of death and severe disability. The course of TBI and SCI has two consecutive poorly demarcated phases: the initial, primary injury and secondary injury. Recent evidence has implicated the role of the CX3CL1/CX3CR1 axis in neuroinflammatory processes occurring after CNS injuries. The importance of the CX3CL1/CX3CR1 axis in the pathophysiology of TBI and SCI in the context of systemic and direct local immune response is still under investigation. This paper, based on a review of the literature, updates and summarizes the current knowledge about CX3CL1/CX3CR1 axis involvement in TBI and SCI pathogenesis, indicating possible molecular and cellular mechanisms with a potential target for therapeutic intervention.
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Registered trials
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.