ArticleThe journal of headache and pain2025
The P2Y13 receptor-mediated microglial morphological transformation through the p38MAPK signaling pathway contributes to central sensitization in a murine model of chronic migraine.
Article in The journal of headache and pain, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The mechanism of different microglial receptors mediating central inflammation in chronic migraine: a meta-analysis.The journal of headache and pain · 2026Pooled it
- Gut microbiota dysbiosis and metabolic reprogramming in pediatric migraine: a multi-omics analysis revealing diagnostic biomarkers.The journal of headache and pain · 2026Article
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11 authors.
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Abstract
backgroundCentral sensitization is a crucial pathophysiological mechanism of chronic migraine (CM), and neuroinflammation mediated by activated microglia contributes significantly to the development of central sensitization. The P2Y13 receptor (P2Y13R), belonging to the G protein-coupled receptor family, is expressed in microglia and actively participates in the intricate pathophysiological process underlying chronic neuropathic pain. However, the precise relationship between the P2Y13R and CM remains largely unclear.
methodsThe CM mouse model was established by repeatedly injecting nitroglycerin (NTG) intraperitoneally at intermittent intervals, and the pain threshold was assessed using von Frey fiber and hot plate tests. Specific interventions were conducted on the P2Y13R and p38 MAPK signaling pathways in the Trigeminal Nucleus Caudalis (TNC) of mice through stereotactic injection. Western blotting and immunofluorescence were employed to assess the expression and localization of P2Y13R, c-Fos, calcitonin gene-related peptide (CGRP), components of the p38 MAPK signaling pathway, and inflammatory factors.
resultsThe expression of P2Y13R was significantly upregulated upon NTG administration and exhibited a predominant distribution within the microglia in the TNC in mice with CM. Pharmacological inhibition of P2Y13R effectively reduced hyperalgesia in CM mice, lowered CGRP and c-fos levels, thereby improving central sensitization. Furthermore, inhibiting P2Y13R suppressed microglial activation and pro-inflammatory cytokine production. Additionally, activation of the p38MAPK pathway was observed in the TNC of CM mice, with P2Y13R inhibition significantly reducing p38MAPK pathway activity. Pharmacological inhibition of p38MAPK significantly ameliorates central sensitization in CM mice, while suppressing microglial activation and pro-inflammatory cytokine levels.
conclusionsThis research emphasizes the significance of P2Y13R in mediating central sensitization in CM mice through the p38MAPK pathway, thereby suggesting that targeting P2Y13R holds promise as a potential therapeutic strategy for effectively managing CM.
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