一种针对疼痛感觉的Nav1.7的方法。

Theodore R Cummins
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引用次数: 0

摘要

疼痛是一种严重的疾病,目前的治疗方法仍然受到副作用的限制。Nav1.7电压门控钠通道是伤害感受器兴奋性的关键决定因素,也是非成瘾性镇痛药物的一个有希望的靶点。然而,阻滞剂的开发一直很困难。在本期JCI中,Singh、Bernabucci和作者确定了降低Nav1.7电流的策略。这些发现确定了成纤维细胞生长因子13 (FGF13),这是一种与典型生长因子(也称为FHF2B)不同的同源因子,可提高Nav1.7,伤害感受器兴奋性和疼痛。化合物PW164被鉴定为具有镇痛活性的选择性FGF13-Nav1.7衰减剂。这些发现强调了靶向Nav1.7的内在调节剂在疼痛管理中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
An approach to targeting Nav1.7 for pain sensations.
Pain is a serious medical condition with current treatments remaining limited by side effects. The Nav1.7 voltage-gated sodium channel is a crucial determinant of nociceptor excitability and a promising target for nonaddictive analgesics. However, development of blockers has been difficult. In this issue of the JCI, Singh, Bernabucci, and authors identify a strategy for reducing Nav1.7 currents. These findings identify fibroblast growth factor 13 (FGF13), a homologous factor distinct from typical growth factors (also known as FHF2B), which ramps up Nav1.7, nociceptor excitability, and pain. Compound PW164 was identified as a selective FGF13-Nav1.7 attenuator with analgesic activity. These findings highlight the power of targeting intrinsic modulators of Nav1.7 for pain management.
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