ArticleThe Journal of experimental medicine2023
Targeting neuroinflammation in neuropathic pain and opioid use.
Article in The Journal of experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Propofol attenuates pain hypersensitivity and neuroinflammation in chronic constriction injury rats by regulating miR-1249-3p/VEGFA axis.The Korean journal of pain · 2026Article
- Iridoids from Traditional Chinese Medicine for Neuropathic Pain: Therapeutic Potential and Molecular Mechanisms.Drug design, development and therapy · 2026Review
- Aloysia oblanceolata Moldenke essential oil exhibits antinociceptive activity regulated by opioids, serotonergic, and α2-adrenergic receptors, along with low toxicity and anti-inflammatory effects.Inflammopharmacology · 2025Article
- Analgesic Mechanism of Emodin in Neuropathic Pain Through Inhibiting P2X4 Purinoceptor Signaling.Molecular neurobiology · 2025Article
- Environmental enrichment for neuropathic pain via modulation of neuroinflammation.Frontiers in molecular neuroscience · 2025Review
- The analgesic mechanism of electroacupuncture at the central level for neuropathic pain: a review of studies based on animal experiments.Frontiers in neurology · 2025Review
- 18 kDa Translocator protein (TSPO) is upregulated in rat brain after peripheral nerve injury and downregulated by diroximel fumarate.Brain, behavior, and immunity · 2025Article
- New Insight into Neuropathic Pain: The Relationship between α7nAChR, Ferroptosis, and Neuroinflammation.International journal of molecular sciences · 2024Review
- Dysregulation of sphingolipid metabolism in pain.Frontiers in pharmacology · 2024Review
- Identification of m1A/m6A/m5C/m7G-related genes and clusters associated with neuropathic pain.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Neuropathic pain arises from injuries to the nervous system. It affects 20% of the adult US population and poses a major socioeconomic burden yet remains exceedingly difficult to treat. Current therapeutic approaches have limited efficacy and a large side effect profile that impedes their ability to treat neuropathic pain effectively. Preclinical research over the last 30 yr has established the critical role that pro-inflammatory neuro-immune cell interactions have in the development and maintenance of neuropathic pain arising from various etiologies. Pro-inflammatory neuro-immune cell interactions also underlie the development of adverse side effects of opioids and the loss of their efficacy to treat pain. Evidence from work in our lab and others in preclinical animal models have shown that signaling from the bioactive sphingolipid, sphingosine-1-phosphate (S1P), through the S1P receptor subtype 1 (S1PR1) modulates neuro-immune cell interactions. Here, we discuss how targeting S1P/S1PR1 signaling with S1PR1 antagonists already Food and Drug Administration-approved or in clinical trials for multiple sclerosis can provide a viable pharmacotherapeutic approach to reduce neuro-immune cell inflammatory signaling and potentially treat patients suffering neuropathic pain and the adverse effects of opioids.
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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.