作者: John J. Haddad
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摘要: Inflammatory cells and inflammatory mediators are crucially involved in the genesis, persistence severity of pain following trauma, infection or nerve injury. The mechanisms pathways mediating nociception transcriptionally regulated. transcriptional mediator nuclear factor (NF)-κB plays a major role regulating milieu, ostensibly via control gene expression/suppression. An association has recently emerged to establish possible link between NF-κB pain/nociception, purportedly through regulation loop secretion (biosynthesis) pro-inflammatory mediators. Current concepts conspicuously indicate that effective inhibition this transcription associated upstream kinase(s) regulate its translocation could be targets new strategy for alleviation inflammation inflammatory-related pain. To better understand relationship NFκB evolution hyperalgesia/nociception, it is imperative unravel molecular basis process. This survey definitively integrates current themes pertaining pivotal shares decoding implicated signaling mechanisms.