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TRPV1 and TRPA1 in cutaneous neurogenic and chronic inflammation: pro-inflammatory response induced by their activation and their sensitization

机译:皮肤神经性和慢性炎症中的TRPV1和TRPA1:活化和敏化引起的促炎反应

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摘要

Cutaneous neurogenic inflammation (CNI) is inflammation that is induced (or enhanced) in the skin by the release of neuropeptides from sensory nerve endings. Clinical manifestations are mainly sensory and vascular disorders such as pruritus and erythema. Transient receptor potential vanilloid 1 and ankyrin 1 (TRPV1 and TRPA1, respectively) are non-selective cation channels known to specifically participate in pain and CNI. Both TRPV1 and TRPA1 are co-expressed in a large subset of sensory nerves, where they integrate numerous noxious stimuli. It is now clear that the expression of both channels also extends far beyond the sensory nerves in the skin, occuring also in keratinocytes, mast cells, dendritic cells, and endothelial cells. In these non-neuronal cells, TRPV1 and TRPA1 also act as nociceptive sensors and potentiate the inflammatory process. This review discusses the role of TRPV1 and TRPA1 in the modulation of inflammatory genes that leads to or maintains CNI in sensory neurons and non-neuronal skin cells. In addition, this review provides a summary of current research on the intracellular sensitization pathways of both TRP channels by other endogenous inflammatory mediators that promote the self-maintenance of CNI.
机译:皮肤神经源性炎症(CNI)是通过从感觉神经末梢释放神经肽而在皮肤中诱发(或增强)的炎症。临床表现主要是感觉和血管疾病,例如瘙痒和红斑。瞬态受体电位香草醛1和锚蛋白1(分别为TRPV1和TRPA1)是已知专门参与疼痛和CNI的非选择性阳离子通道。 TRPV1和TRPA1都在大量的感觉神经中共表达,它们整合了许多有害刺激。现在清楚的是,这两个通道的表达还远远超出了皮肤中的感觉神经,还存在于角质形成细胞,肥大细胞,树突状细胞和内皮细胞中。在这些非神经元细胞中,TRPV1和TRPA1还充当伤害感受器并增强炎症过程。这篇综述讨论了TRPV1和TRPA1在调节导致或维持感觉神经元和非神经元皮肤细胞中CNI的炎症基因中的作用。此外,本综述提供了当前其他研究的摘要,这些研究涉及促进CNI自我维持的其他内源性炎症介质对两个TRP通道的细胞内致敏途径。

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