J Clin Invest. 2024 May 1;134(9):e180497. doi: 10.1172/JCI180497.
Pain and inflammation are biologically intertwined responses that warn the body of potential danger. In this issue of the JCI, Defaye, Bradaia, and colleagues identified a functional link between inflammation and pain, demonstrating that inflammation-induced activation of stimulator of IFN genes (STING) in dorsal root ganglia nociceptors reduced pain-like behaviors in a rodent model of inflammatory pain. Utilizing mice with a gain-of-function STING mutation, Defaye, Bradaia, and colleagues identified type I IFN regulation of voltage-gated potassium channels as the mechanism of this pain relief. Further investigation into mechanisms by which proinflammatory pathways can reduce pain may reveal druggable targets and insights into new approaches for treating persistent pain.
疼痛和炎症是生物上相互交织的反应，它们警告身体潜在的危险。在本期 JCI 中，Defaye、Bradaia 和同事们发现了炎症和疼痛之间的功能联系，证明了炎症诱导的干扰素基因刺激物 (STING) 在背根神经节伤害感受器中的激活，减少了炎症性疼痛模型中类似疼痛的行为。利用具有 STING 基因突变的功能获得型小鼠，Defaye、Bradaia 和同事们确定了 I 型干扰素对电压门控钾通道的调节是这种疼痛缓解的机制。对促炎途径如何减轻疼痛的机制的进一步研究可能会揭示可用药的靶点，并为治疗持续性疼痛提供新的方法。
