Xin Long, Xu Wei-Xing, Wang Jian, Song Hong-Pu, Liu Jian, Wang Jin, Fan Shun-Wu, Yang Yang
Department of Orthopaedics, Tongde Hospital of Zhejiang Province, Hangzhou 310012, Zhejiang, China.
Zhongguo Gu Shang. 2021 Jun 25;34(6):589-92. doi: 10.12200/j.issn.1003-0034.2021.06.021.
Nonspecific low back pain is closely associated with afferent nerve ingrowth into degenerated IVDs and increasing the inflammatory response. Members of the class 3 semaphorins signal their response through two prominent receptors; the NRP (Neuropilin-1) and the Plexin A. Sema3A (Semaphorin3A) is primarily known for their role in modulating neuronal survival as well as neurite outgrowth and guidance via regulation of Sema3A-NRP-1-plexinA signal pathway. Also, sema3A is shown to be conductive to innervate the inner painful degenerated IVDs (Intervertebral discs). Furthermore, sema3A is thought to act as a barrier to endothelial cells survival and migration on vascular endothelial growth factor (VEGF) and inhibition of KLF5-induced (Krüppel-like factor 5) inflammatory mediators within degenerated IVDs. Therefore, Sema3A produce a new perspective of dual-action therapeutic agent for attenuating the regulator of innervation and angiogenesis into degenerated IVDs and inhibition of KLF5-induced inflammation.
非特异性下腰痛与传入神经长入退变的椎间盘并增强炎症反应密切相关。3类信号素成员通过两种主要受体发出反应信号；即神经纤毛蛋白（Neuropilin-1）和丛状蛋白A。信号素3A（Semaphorin3A）主要因其通过调节信号素3A-神经纤毛蛋白-1-丛状蛋白A信号通路在调节神经元存活以及神经突生长和导向方面的作用而闻名。此外，信号素3A被证明有助于支配退变的椎间盘内部产生疼痛。此外，信号素3A被认为对血管内皮生长因子（VEGF）作用下的内皮细胞存活和迁移起屏障作用，并抑制退变椎间盘中Krüppel样因子5（KLF5）诱导的炎症介质。因此，信号素3A为减轻退变椎间盘中神经支配和血管生成的调节以及抑制KLF5诱导的炎症提供了一种双作用治疗剂的新视角。
