ArticlePain2018
Chemokine (c-c motif) receptor 2 mediates mechanical and cold hypersensitivity in sickle cell disease mice.
Article in Pain, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Dyslipidemia is a metabolic hallmark of acute pain in sickle cell disease.medRxiv : the preprint server for health sciences · 2026Article
- Dual CCR2/CCR5 Antagonism with Cenicriviroc Alleviates Nerve Injury-Induced Hypersensitivity and Prevents Morphine Tolerancevia Modulation of Neuroimmune Signaling.Cellular and molecular neurobiology · 2026Article
- An Integrated Multi-Tissue Single-Cell Transcriptomic Analysis Highlights the CCL2-CCR2 Signaling Pathway as a Potential Therapeutic Target in Neuropathic Pain.Journal of pain research · 2026Article
- Gut microbiota and metabolites drive chronic sickle cell disease pain in mice.Cell host & microbe · 2025Article
- Molecular inflammatory expression profiles associated with the frequency of pain in individuals with sickle cell disease.Blood advances · 2025Article
- Biomarker signatures for sickle cell pain.Blood advances · 2025Article
- Article
- Mast cell extracellular trap formation underlies vascular and neural injury and hyperalgesia in sickle cell disease.Life science alliance · 2024Article
- A humanized focus on sickle cell pain.Blood · 2024Article
- Article
- Article
- Descending Facilitation of Nociceptive Transmission From the Rostral Ventromedial Medulla Contributes to Hyperalgesia in Mice with Sickle Cell Disease.Neuroscience · 2023Article
- The Complex Association of Daily Opioid Dose with Visits for Pain in Sickle Cell Disease: Tolerance or Treatment-Refractory Pain?Pain medicine (Malden, Mass.) · 2023Observational
- Distinct Mechanisms Account for In Vitro Activation and Sensitization of TRPV1 by the Porphyrin Hemin.International journal of molecular sciences · 2021Article
- Transient receptor potential canonical 5 mediates inflammatory mechanical and spontaneous pain in mice.Science translational medicine · 2021Article
- Nociceptors protect sickle cell disease mice from vaso-occlusive episodes and chronic organ damage.The Journal of experimental medicine · 2021Article
- Neuropathic Pain and Sickle Cell Disease: a Review of Pharmacologic Management.Current pain and headache reports · 2020Review
- End points for sickle cell disease clinical trials: patient-reported outcomes, pain, and the brain.Blood advances · 2019Article
- Female-Specific Effects of CGRP Suggest Limited Efficacy of New Migraine Treatments in Males.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Updated mechanisms underlying sickle cell disease-associated pain.Neuroscience letters · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Approximately one-third of individuals with sickle cell disease (SCD) develop chronic pain. This debilitating pain is inadequately treated because the underlying mechanisms driving the pain are poorly understood. In addition to persistent pain, patients with SCD are also in a tonically proinflammatory state. Previous studies have revealed that there are elevated plasma levels of many inflammatory mediators including chemokine (c-c motif) ligand 2 (CCL2) in individuals with SCD. Using a transgenic mouse model of SCD, we investigated the contributions of CCL2 signaling to SCD-related pain. Inhibition of chemokine receptor 2 (CCR2), but not CCR4, alleviated the behavioral mechanical and cold hypersensitivity in SCD. Furthermore, acute CCR2 blockade reversed both the behavioral and the in vitro responsiveness of sensory neurons to an agonist of TRPV1, a neuronal ion channel previously implicated in SCD pain. These results provide insight into the immune-mediated regulation of hypersensitivity in SCD and could inform future development of analgesics or therapeutic measures to prevent chronic pain.
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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.