ReviewMolecular neurobiology2020
Mechanisms for Reducing Neuropathic Pain.
Review in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis 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
28 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Platelet-rich Plasma for the Treatment of Neuropathic Pain: A Systematic Review.Current drug research reviews · 2025Pooled it
- Lappaconitine protects SH-SY5Y cells from TNF-α-induced mitochondrial apoptosis by blocking the Bax-dependent Caspase-3 signaling pathway.Scientific reports · 2026Article
- Article
- Potential Effect of Intravesical Platelet-Rich Plasma Injection on Urinary Retention: A Case Report.Clinical case reports · 2025Article
- Oxidative Stress, Inflammation, and Cellular Senescence in Neuropathic Pain: Mechanistic Crosstalk.Antioxidants (Basel, Switzerland) · 2025Review
- Amelioration of Freund's adjuvant-induced polyarthritis by Diosmin-loaded nanoparticles in Wistar rats; a mechanistic study.Inflammopharmacology · 2025Article
- Frequency of central sensitization and nociplastic pain in patients with plantar fasciitis : Central sensitization and nociplastic pain in plantar fasciitis.International orthopaedics · 2025Article
- N-Demethylsinomenine Relieves Neuropathic Pain in Male Mice Mainly via Regulating α2-Subtype GABACNS neuroscience & therapeutics · 2025Article
- Ultrasound-guided perineural intercostal autologous platelet-rich plasma in the treatment of chronic post-thoracotomy pain syndrome - A prospective case series.Interventional pain medicine · 2024Article
- Down-regulation of microRNA-382-5p reduces neuropathic pain by targeting regulation of dual specificity phosphatase-1.The Korean journal of pain · 2024Article
- The Antinociceptive Role of Nrf2 in Neuropathic Pain: From Mechanisms to Clinical Perspectives.Pharmaceutics · 2024Review
- Tannic acid inhibits pain mediators, inflammation and oxidative stress in mice exposed to glyphosate-based herbicide.Environmental analysis, health and toxicology · 2024Article
- Tumor Necrosis Factor and Interleukin Modulators for Pathologic Pain States: A Narrative Review.Pain and therapy · 2024Review
- TLR4 induced TRPM2 mediated neuropathic pain.Frontiers in pharmacology · 2024Review
- Serum Inflammatory Cytokine Levels in Herpes Zoster Patients and Their Association with Postherpetic Neuralgia: A Prospective Study.Medical science monitor : international medical journal of experimental and clinical research · 2023Article
- Targeting Anti-Inflammatory Pathways to Treat Diabetes-Induced Neuropathy by 6-Hydroxyflavanone.Nutrients · 2023Article
- Evolving techniques for reducing phantom limb pain.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Through Its Powerful Antioxidative Properties, L-Theanine Ameliorates Vincristine-Induced Neuropathy in Rats.Antioxidants (Basel, Switzerland) · 2023Article
- P-Selectin is a Critical Factor for Platelet-Mediated Protection on Restraint Stress-Induced Gastrointestinal Injury in Mice.International journal of molecular sciences · 2022Article
- Neuroimmune Mechanisms Underlying Neuropathic Pain: The Potential Role of TNF-α-Necroptosis Pathway.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Injury typically results in the development of neuropathic pain, but the pain normally decreases and disappears in paralleled with wound healing. The pain results from cells resident at, and recruited to, the injury site releasing pro-inflammatory cytokines and other mediators leading to the development of pro-inflammatory environment and causing nociceptive neurons to develop chronic ectopic electrical activity, which underlies neuropathic pain. The pain decreases as some of the cells that induce pro-inflammation, changing their phenotype leading to the blocking the release of pro-inflammatory mediators while releasing anti-inflammatory mediators, and blocking nociceptive neuron chronic spontaneous electrical activity. Often, despite apparent wound healing, the neuropathic pain becomes chronic. This raises the question of how chronic pain can be eliminated. While many of the cells and mediators contributing to the development and maintenance of neuropathic pain are known, a better understanding is required of how the injury site environment can be controlled to permanently eliminate the pro-inflammatory environment and silence the chronically electrically active nociceptive neurons. This paper examines how methods that can promote the transition of the pro-inflammatory injury site to an anti-inflammatory state, by changing the composition of local cell types, modifying the activity of pro- and anti-inflammatory receptors, inducing the release of anti-inflammatory mediators, and silencing the chronically electrically active nociceptive neurons. It also examines the hypothesis that factors released from platelet-rich plasma applied to chronic pain sites can permanently eliminate chronic inflammation and its associated chronic pain.
Indexed as
Identifiers
31813127What 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.