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Fig. 2 | The Journal of Headache and Pain

Fig. 2

From: Migraine and neuroinflammation: the inflammasome perspective

Fig. 2

New era for migraine: Inflammasome activation as a treatment target or a biomarker. In the background of genetically hyperexcitable brain, triggering factors induce CSD which results in Pannexin-1 megachannel opening and K+ efflux from P2X7R, consequently creates stress on the cell. Reactive oxygen species (ROS) from membranous Arachidonic acid (AA) and mitochondria respond to this cellular stress via mtROS production which is sensed by mtDNA and TXNIP. K+ efflux, mtDNA and Pannexin-1 megachannel opening cause the assembly of inflammasome complex elements (NLRP3, ASC, pro-caspase-1) and activation of caspase-1 which cleaves pro forms of IL-1╬▓ and IL-18 and ignites parenchymal neuroinflammatory signaling to alert adjacent cells. This cascade eventually reaches the trigeminovascular system around meningeal vessels which results in activation of this system and consequently headache. COVID-19 viroporins induce NLRP3 inflammasome formation via increase in mitochondrial ROS production. This may be an overlapping mechanism in migraine and COVID-19 headache. On the contrary, ACh, main actor in cholinergic anti-inflammatory pathway, inhibits NLRP3 inflammasome by decreasing mtDNA release through binding to mitochondrial ╬▒7 nAChR

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