ArticleCNS neuroscience & therapeutics2025
CXCL10 Involvement in Vestibular Migraine via the PI3K/AKT Signaling Pathway.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- CXCL10 knockdown attenuates vestibular migraine in rats by inhibiting PI3K-mediated neuroinflammation and central sensitization.The journal of headache and pain · 2026Article
- Cathepsin C Restricts Influenza A Virus Replication and Is Associated with Suppression of the PI3K-AKT Signaling Pathway.Viruses · 2026Article
- TREM2 contributes to central sensitization through PI3K/Akt/mTOR-mediated autophagic dysfunction in a rat model of vestibular migraine.The journal of headache and pain · 2026Article
- CXCL10 Involvement in Vestibular Migraine via the PI3K/AKT Signaling Pathway.CNS neuroscience & therapeutics · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
aimsC-X-C motif chemokine ligand 10 (CXCL10) is a member of the CXC chemokine family, known as a classical pain-related chemokine. While CXCL10 is implicated in neuropathic pain, its role in vestibular migraine (VM) remains unclear.
methodsSerum CXCL10 levels correlated with dizziness and headache severity in VM patients. In the rat VM model, CXCL10, C-X-C motif chemokine receptor 3 (CXCR3), and phosphatidylinositol 4,5-bisphosphate 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway expression were evaluated to explore the potential mechanisms of CXCL10 in VM.
resultsSerum CXCL10 levels in VM patients were significantly elevated and positively correlated with headache and dizziness severity. In the rat VM model, CXCL10 and CXCR3 expression in the trigeminal nucleus caudalis and vestibular nuclei were significantly increased. Additionally, molecules related to the PI3K/AKT signaling pathway and downstream inflammatory factors showed significantly elevated expression.
conclusionCXCL10 activates the PI3K/AKT signaling pathway, promoting the release of inflammatory factors, including interleukin-1β, interleukin-6, and tumor necrosis factor-α, and is thus involved in the pathogenesis of VM.
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