ReviewInternational journal of molecular sciences2017
Pharmacological Regulation of Neuropathic Pain Driven by Inflammatory Macrophages.
Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 4 of them syntheses that pooled it.
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
57 citing papers in PubMed, 4 syntheses or guidelines pooled it, 104 citations in OpenAlex.
- Systematic Review: Preclinical and Clinical Evidence on MSC Efficacy and Mechanism of Action in Neuropathic Pain Reduction.International journal of molecular sciences · 2026Pooled it
- Relationship between BMI and chemotherapy-induced peripheral neuropathy in cancer patients: a dose-response meta-analysis.World journal of surgical oncology · 2025Pooled it
- The involvement and significance of M2 macrophages in neuropathic pain following spinal cord injury: a systematic review.The journal of physiological sciences : JPS · 2024Pooled it
- Progress in Pathological and Therapeutic Research of HIV-Related Neuropathic Pain.Cellular and molecular neurobiology · 2023Pooled it
- CGRP-provoked headache is associated with a neuroimmune signature in idiopathic intracranial hypertension.The journal of headache and pain · 2026Trial
- Glial Activation Enhances Spinal TRPV1 Receptor Sensitivity in a Paclitaxel Model of Neuropathic Pain.Physiological research · 2025Article
- The Neuroregenerative Effects of IncobotulinumtoxinA (Inco/A) in a Nerve Lesion Model of the Rat.International journal of molecular sciences · 2025Article
- Hyperalgesia in the Psychological Stress-Induced Fibromyalgia Model Shows Sexual Dimorphism Mediated by LPACells · 2025Article
- HDAC6 inhibition ameliorates sensory hypersensitivity and reduces immune cell signatures in the dorsal root ganglia in murine chronic pain models.Molecular pharmacology · 2025Article
- Unraveling proteomic signatures and neuroinflammatory networks in a CCI rat model of early sciatica: insights for neuropathic pain mechanisms.Frontiers in molecular neuroscience · 2025Article
- Discovery of Antinociceptive α9α10 Nicotinic Acetylcholine Receptor Antagonists by Stable Receptor Expression.ACS chemical biology · 2024Article
- Exploring the Therapeutic Potential of Mesenchymal Stem Cells-derived conditioned medium: An In-depth Analysis of Pain Alleviation, Spinal CCL2 Levels, and Oxidative Stress.Cell biochemistry and biophysics · 2024Article
- Myeloid Cell Association with Spinal Cord Injury-Induced Neuropathic Pain and Depressive-like Behaviors in LysM-eGFP Mice.The journal of pain · 2024Article
- Causal links between blood inflammation markers and postherpetic neuralgia risk: insights from a two-sample Mendelian randomization study.Frontiers in neurology · 2024Article
- A review of the current state in neointimal hyperplasia development following endovascular intervention and minor emphasis on new horizons in immunotherapy.Translational and clinical pharmacology · 2023Review
- Peripheral neuropathy associated with monomethyl auristatin E-based antibody-drug conjugates.iScience · 2023Review
- Cryo-EM structures of human GPR34 enable the identification of selective antagonists.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The Role of Immune Mechanisms in Abdominal Aortic Aneurysm: Could It be a Promising Therapeutic Strategy?Acta Cardiologica Sinica · 2023Review
- Microglia polarization in nociplastic pain: mechanisms and perspectives.Inflammopharmacology · 2023Review
- Neutrophils infiltrate sensory ganglia and mediate chronic widespread pain in fibromyalgia.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain can have a major effect on quality of life but current therapies are often inadequate. Growing evidence suggests that neuropathic pain induced by nerve damage is caused by chronic inflammation. Upon nerve injury, damaged cells secrete pro-inflammatory molecules that activate cells in the surrounding tissue and recruit circulating leukocytes to the site of injury. Among these, the most abundant cell type is macrophages, which produce several key molecules involved in pain enhancement, including cytokines and chemokines. Given their central role in the regulation of peripheral sensitization, macrophage-derived cytokines and chemokines could be useful targets for the development of novel therapeutics. Inhibition of key pro-inflammatory cytokines and chemokines prevents neuroinflammation and neuropathic pain; moreover, recent studies have demonstrated the effectiveness of pharmacological inhibition of inflammatory (M1) macrophages. Nicotinic acetylcholine receptor ligands and T helper type 2 cytokines that reduce M1 macrophages are able to relieve neuropathic pain. Future translational studies in non-human primates will be crucial for determining the regulatory mechanisms underlying neuroinflammation-associated neuropathic pain. In turn, this knowledge will assist in the development of novel pharmacotherapies targeting macrophage-driven neuroinflammation for the treatment of intractable neuropathic pain.
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What OpenQuestion holds
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.