ArticleRegional anesthesia and pain medicine2026
Elevated 18:1 lysophosphatidylcholine contributes to neuropathic pain in peripheral nerve injury.
Article in Regional anesthesia and pain medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Serum Lipidomics Profiling Identify Novel Biomarkers of Distal Symmetrical Polyneuropathy in Type 1 Diabetes.Diabetes, obesity & metabolism · 2026Article
- PM2.5 Exacerbates Viral Myocarditis by Disrupting Lysophosphatidylcholine Metabolism and Inhibiting the GPR4/ERK/PPARγ Pathway.Journal of applied toxicology : JAT · 2026Article
- LPC18:0 Secreted by Exogenous Neural Stem Cells Potentiates Neurogenesis and Functional Recovery via GPR55-Mediated Signalling in Spinal Cord Injury.Cell proliferation · 2026Article
- Hyodeoxycholic acid relieves neuropathic pain by activating farnesoid X receptor signaling.Journal of advanced research · 2026Article
- Transcriptome profiling suggests molecular sexual dimorphism in lumbosacral dorsal root ganglia and sex-specific mechanisms underlying visceral pain.Physiological genomics · 2026Article
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Authors and funding
12 authors.
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Abstract
backgroundNeuropathic pain is a maladaptive and chronic condition with limited effective treatments. Although recent studies have suggested that certain lipid metabolites, like lysophosphatidylcholine (LPC), may contribute to chronic pain, their specific roles and mechanisms remain unclear.
objectiveThis study investigated the role and mechanism of LPC(18:1), a lipid subtype, in neuropathic pain caused by nerve injury.
methodsUsing a mouse model of spinal nerve ligation, LPC(18:1) levels were measured in serum, dorsal root ganglion (DRG), spinal cord (SC) and cerebrospinal fluid (CSF). Nociception was assessed using von Frey and Hargreaves' methods, while molecular analyses explored inflammatory pathways and oxidative stress.
resultsLPC(18:1) levels significantly increased in the serum, DRG and CSF after nerve injury. Administration of LPC(18:1) induced heightened pain responses and activated inflammatory pathways, including protein kinase C (PKC) and extracellular regulated protein kinase (ERK) in the DRG, as well as glial cells in the SC. The findings suggested that oxidative stress played a role in LPC(18:1) production, and its effects were mediated by G protein-coupled receptor 132 (GPR132).
conclusionLPC(18:1) may serve as a potential biomarker and therapeutic target for managing neuropathic pain.
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