ReviewBiomedicines2025
The Role of the CCR5 Receptor in Neuropathic Pain Modulation: Current Insights and Therapeutic Implications.
Review in Biomedicines, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Sex-specific lateralization of the effects of exogenously-induced neuroimmune activation in the amygdala on pain-like behaviors.Frontiers in pharmacology · 2026Article
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain, a chronic condition arising from injury or dysfunction of the somatosensory nervous system, is characterized by persistent hypersensitivity and spontaneous pain. The chemokine receptor CCR5 (C-C motif chemokine receptor 5) has recently been identified as a critical mediator in neuroinflammation and neuropathic pain signaling pathways. Expressed on immune cells and neurons, CCR5 regulates immune cell recruitment and activation, thereby contributing to neuronal sensitization and maintenance of pain states. This review examines the currently characterized molecular mechanisms through which CCR5 modulates neuropathic pain pathophysiology and assesses the potential of CCR5 antagonists as novel therapeutic agents for the management of chronic neuropathic pain. Understanding the involvement of CCR5 in pain modulation may facilitate the development of targeted treatments with improved efficacy and safety profiles.
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