Persistent pain, which is poorly treated and estimated to afflict one third of the world's population, is largely mediated by the sensitization of nociceptive neurons. This sensitization involves de novo gene expression to support biochemical and structural changes required to maintain amplified pain signaling that frequently persists even after injury to tissue resolves. While transcription-dependent changes in gene expression are important, recent work demonstrates that activity-dependent regulation of mRNA translation is key to controlling the cellular proteome and the development and maintenance of persistent pain. In this review, we highlight recent advances in translational regulation of gene expression in nociceptive circuits, with a focus on key signaling pathways and mRNA targets that may be tractable for the creation of next-generation pain therapeutics.

中文翻译：

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持续性疼痛的转化控制机制

持续性疼痛治疗效果不佳，据估计困扰着世界三分之一的人口，主要是由伤害感受神经元的敏化介导的。这种敏化涉及从头基因表达，以支持维持放大的疼痛信号所需的生化和结构变化，即使在组织损伤消退后，疼痛信号也经常持续存在。虽然基因表达的转录依赖性变化很重要，但最近的工作表明，mRNA 翻译的活性依赖性调节是控制细胞蛋白质组以及持续性疼痛的发展和维持的关键。在这篇综述中，我们强调了伤害感受回路中基因表达的翻译调控的最新进展，