Cell signaling pathways related to pain receptors in the degenerated disk.
Cell signaling pathways related to pain receptors in the degenerated disk.
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DOI：
10.1055/s-0033-1345036
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发表时间：
2013-06
影响因子：
2.4
通讯作者：
Mochida J
中科院分区：
文献类型：
--
作者：
Hiyama A;Sakai D;Mochida J
下背痛的许多原因仍然未知;足够的证据表明椎间盘（IVD）内的退行性和机械性变化是一个相关因素。本文就退变椎间盘中与疼痛受体相关的细胞内信号通路作一综述。一些报告已经证明，椎间盘退变时椎间盘内的神经纤维数量增加。近年来，一些研究小组报告称，神经纤维的增加与IVD中炎症介质和/或神经营养因子的存在有关。必须识别受炎症介质和神经营养因子调节的细胞信号传导事件，以阐明腰痛的潜在机制。主要的细胞内信号传导途径（核因子κ β、促分裂原活化蛋白激酶和Wnt）可能在介导导致IVD变性开始和进展的分子事件中发挥重要作用。这些信号通路可能代表治疗IVD变性及其相关背痛的治疗靶点。
Many of the causes of low back pain are still unknown; sufficient evidence indicates that both degenerative and mechanical change within the intervertebral disk (IVD) is a relevant factor. This article reviews intracellular signaling pathways related to pain receptors in the degenerated IVD. Several reports have demonstrated the number of nerve fibers in the IVD was increased in degenerated disks. In recent years, some groups have reported that an increase in nerve fibers is associated with the presence of inflammatory mediators and/or neurotrophins in the IVD. Cell signaling events, which are regulated by inflammatory mediators and neurotrophins, must be identified to clarify the mechanism underlying low back pain. Major intracellular signaling pathways (nuclear factor kappa β, mitogen-activated protein kinases, and Wnts) potentially play vital roles in mediating the molecular events responsible for the initiation and progression of IVD degeneration. These signaling pathways may represent therapeutic targets for the treatment of IVD degeneration and its associated back pain.
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影响因子：
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作者：
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