p38 MAPK, Microglial Signaling, and Neuropathic Pain

p38 MAPK, Microglial Signaling, and Neuropathic Pain

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p38 MAPK, Microglial Signaling, and Neuropathic Pain

dc.contributor.author	Ji, Ru-Rong
dc.contributor.author	Suter, Marc
dc.date.accessioned	2011-05-07T23:47:37Z
dc.date.issued	2007
dc.identifier.citation	Ji, Ru-Rong, and Marc R Suter. 2007. p38 MAPK, microglial signaling, and neuropathic pain. Molecular Pain 3: 33.	en_US
dc.identifier.issn	1744-8069	en_US
dc.identifier.uri	http://nrs.harvard.edu/urn-3:HUL.InstRepos:4882980
dc.description.abstract	Accumulating evidence over last several years indicates an important role of microglial cells in the pathogenesis of neuropathic pain. Signal transduction in microglia under chronic pain states has begun to be revealed. We will review the evidence that p38 MAPK is activated in spinal microglia after nerve injury and contributes importantly to neuropathic pain development and maintenance. We will discuss the upstream mechanisms causing p38 activation in spinal microglia after nerve injury. We will also discuss the downstream mechanisms by which p38 produces inflammatory mediators. Taken together, current data suggest that p38 plays a critical role in microglial signaling under neuropathic pain conditions and represents a valuable therapeutic target for neuropathic pain management.	en_US
dc.language.iso	en_US	en_US
dc.publisher	BioMed Central	en_US
dc.relation.isversionof	doi://10.1186/1744-8069-3-33	en_US
dc.relation.hasversion	http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2186318/pdf/	en_US
dash.license	LAA
dc.title	p38 MAPK, Microglial Signaling, and Neuropathic Pain	en_US
dc.type	Journal Article	en_US
dc.description.version	Version of Record	en_US
dc.relation.journal	Molecular Pain	en_US
dash.depositing.author	Ji, Ru-Rong
dc.date.available	2011-05-07T23:47:37Z
dash.affiliation.other	HMS^Anaesthesia-Brigham and Women's Hospital	en_US
dash.affiliation.other	HMS^Anaesthesia-Brigham and Women's Hospital	en_US