ArticleCNS neuroscience & therapeutics2024
OTULIN's influence on neuroinflammation and pain modulation in trigeminal neuralgia.
Article in CNS neuroscience & therapeutics, 2024. 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.
- Glymphatic system bridges peripheral and central nervous system changes in classic trigeminal neuralgia.Brain communications · 2026Article
- Insights into the Involvement of TRPA1 Channels in the Neuro-Inflammatory Machinery of Trigeminal Neuralgia.Molecules (Basel, Switzerland) · 2025Article
- Exploring the role of ubiquitination modifications in migraine headaches.Frontiers in immunology · 2025Review
- A narrative review of autophagy in migraine.Frontiers in neuroscience · 2025Review
- OTULIN's influence on neuroinflammation and pain modulation in trigeminal neuralgia.CNS neuroscience & therapeutics · 2024Article
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Authors and funding
8 authors.
Funding
Abstract
introductionTrigeminal neuralgia (TN), marked by chronic pain from neural damage, is closely associated with inflammation. The role of OTULIN, a key regulator in inflammation and autophagy, is not fully understood in TN. The regulatory mechanism of OTULIN, a key protein involved in modulating inflammatory responses and autophagy processes, remains incompletely elucidated, particularly in the context of TN and neuroinflammation.
methodsAn infraorbital nerve ligation-induced rat model of TN was used. OTULIN's expression was modulated using adenovirus vectors and short hairpin RNA. The impact on pain and inflammatory responses was assessed via quantitative real-time polymerase chain reaction, western blot, immunofluorescence, and transcriptomic analysis.
resultsEnhanced OTULIN expression significantly increased head withdrawal thresholds and reduced pain sensitivity and neuroinflammatory markers in the model. Conversely, silencing OTULIN exacerbated pain and inflammation. Transcriptomic data revealed OTULINs influence on both inflammatory and autophagy pathways, specifically in suppressing NLR family pyrin domain containing 3 (NLRP3) inflammasome and promoting autophagy. In vitro experiments demonstrated OTULIN's inhibition of inflammatory markers in microglia and neurons.
conclusionOTULIN is crucial in modulating TN, reducing neuropathic pain and neuroinflammation by activating the autophagy pathway and inhibiting the NLRP3 inflammasome.
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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 Socratic graph.