{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T11:57:06Z","timestamp":1783339026979,"version":"3.54.6"},"reference-count":39,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2025,4,28]],"date-time":"2025-04-28T00:00:00Z","timestamp":1745798400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Synapse"],"published-print":{"date-parts":[[2025,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Migraines profoundly impact patients' quality of life. This study seeks to investigate the relationship between dysregulated miR\u201022\u20103p and the neuroinflammation and central sensitization associated with migraine.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Initially, the level of miR\u201022\u20103p in migraine patients were analyzed using RT\u2010qPCR. Subsequently, a migraine model was established by administering nitroglycerin (NTG) to mice. To modulate the levels of miR\u201022\u20103p within this model, agomir was utilized. Following this intervention, mechanical and thermal pain sensitivity were evaluated by Von Frey filament and radiant heat. The levels of c\u2010Fos, CGRP, TNF\u2010\u03b1, IL\u20101\u03b2, and IL\u20106 in trigeminal nucleus caudalis (TNC) were detected by RT\u2010qPCR and ELISA. Furthermore, dual luciferase reporting assays were conducted to ascertain whether miR\u201022\u20103p could target KLF6. Moreover, the influence of KLF6 on inflammatory cytokines and central sensitization were further studied.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>miR\u201022\u20103p was significantly reduced in migraine patients and NTG mice. In animals, overexpression of miR\u201022\u20103p significantly alleviated hyperalgesia and neuroinflammation induced by NTG. Following the overexpression of miR\u201022\u20103p, we observed an increase in thermal withdrawal latency, paw mechanical threshold, and periorbital mechanical threshold. Conversely, levels of c\u2010Fos, CGRP, TNF\u2010\u03b1, IL\u20101\u03b2, and IL\u20106 exhibited a significant reduction. We found that miR\u201022\u20103p can inhibit KLF6 expression. Additionally, further findings indicated that the suppression of KLF6 resulted in decreased pain sensitivity along with diminished expression of c\u2010Fos, CGRP, TNF\u2010\u03b1, IL\u20101\u03b2, and IL\u20106.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>In the context of migraine, miR\u201022\u20103p may play a pivotal role in mitigating neuroinflammation and alleviating central sensitization through the inhibition of KLF6.<\/jats:p><\/jats:sec>","DOI":"10.1002\/syn.70017","type":"journal-article","created":{"date-parts":[[2025,4,28]],"date-time":"2025-04-28T14:44:19Z","timestamp":1745851459000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Upregulation of miR\u201022\u20103p Alleviates Hyperalgesia and Neuroinflammation Caused by Migraine"],"prefix":"10.1002","volume":"79","author":[{"given":"Lijun","family":"Yang","sequence":"first","affiliation":[{"name":"Department of 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