期刊
MOLECULAR PAIN
卷 3, 期 -, 页码 -出版社
SAGE PUBLICATIONS INC
DOI: 10.1186/1744-8069-3-33
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资金
- FIC NIH HHS [R03 TW007180, TW7180] Funding Source: Medline
- NIDCR NIH HHS [R01 DE017794, DE17794] Funding Source: Medline
- NINDS NIH HHS [R01 NS054932, R01 NS040698, NS40698] Funding Source: Medline
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.
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