ReviewThe Korean journal of pain2026
Microglia-derived neuroinflammatory pathways in neuropathic pain.
Review in The Korean journal of pain, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- Review
- To Prune or to Protect: Complement-Mediated Microglial Synaptic Pruning as a Therapeutic Target in Neuropathic Pain.Molecular neurobiology · 2026Review
- Neuroligins and Neuropathic Pain: Insights into Synaptic Plasticity and Pain Transmission.Biology · 2026Review
- Bioactive compounds for neuroinflammation and neuropathic pain management: molecular and cellular mechanisms.Inflammopharmacology · 2026Review
- Translational stem cell therapy for neurodegeneration and CNS trauma: a focused review.Molecular biology reports · 2026Review
- Metabolic Competition Between Microglia and Neurons as Driver of Chronic Pain.Molecular neurobiology · 2026Review
- Tuina Attenuates Pain with Reduced Serum Pain- and Inflammation-Related Mediators and p38 MAPK Phosphorylation in Selected Brain Regions in Rats with Knee Osteoarthritis.Journal of pain research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain (NP) is a chronic pain condition resulting from damage or disease in the nervous system. It is characterized by hyperalgesia, spontaneous pain, and mechanical allodynia. Due to limited treatment options, NP significantly impairs the quality of life of affected individuals. Recent research has highlighted the critical role of microglia in the initiation and maintenance of NP, however, the underlying mechanisms remain incompletely understood. Existing evidence suggests that signaling pathways, including NF-κB, PI3K/Akt/mTOR, p38MAPK, JAK2/STAT3, and Nrf2/HO-1, contribute to microglial activation and the modulation of NP. This review explores the key activation molecules in these pathways, the microglial phenotype, and associated inflammatory processes. Additionally, the authors summarize the latest literature and application prospects of certain drugs/compounds/ non-invasive treatments, aiming to provide a theoretical basis for the development of novel microglia-targeted therapies.
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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.