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首页> 外文期刊>Expert opinion on therapeutic targets >The ERK/MAPK pathway, as a target for the treatment of neuropathic pain.
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The ERK/MAPK pathway, as a target for the treatment of neuropathic pain.

机译：ERK / MAPK途径，作为治疗神经性疼痛的靶标。

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摘要

Peripheral nerve injury produces neuropathic pain as well as phosphorylation of mitogen activated protein kinase (MAPK) family in dorsal root ganglia (DRG) and dorsal horn. Following nerve injury, phosphorylation of extracellular signal-regulated protein kinase (ERK), an important member of this family, is sequentially increased in neurons, microglia and astrocytes of the dorsal horn and gracile nucleus, and in injured large DRG neurons. Nerve injury-induced phosphorylation of ERK occurs early and is long-lasting. In several animal models of neuropathic pain, MEK inhibitors, known to suppress the synthesis of ERK, have proven effective to alleviate pain at various time points. Thus, the regulation of ERK/MAPK can be considered as a promising therapeutic target for the treatment of neuropathic pain.
机译：周围神经损伤在背根神经节（DRG）和背角中产生神经性疼痛以及丝裂原活化蛋白激酶（MAPK）家族的磷酸化。神经损伤后，背角和细小核的神经元，小胶质细胞和星形胶质细胞，以及受损的大DRG神经元中，细胞外信号调节蛋白激酶（ERK）（该家族的重要成员）的磷酸化依次增加。神经损伤诱导的ERK磷酸化发生得很早，并且持续时间很长。在几种神经性疼痛的动物模型中，MEK抑制剂已知可抑制ERK的合成，已证明可在不同时间点有效缓解疼痛。因此，ERK / MAPK的调节可被视为治疗神经性疼痛的有希望的治疗靶标。

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