伤害感受器
神经病理性疼痛
细胞生物学
下调和上调
伤害
转录组
髓鞘
调节器
神经科学
化学
平衡
核糖核酸酶
慢性疼痛
痛觉过敏
功能(生物学)
炎症
神经损伤
生物
基因表达
P物质
基因表达调控
信使核糖核酸
轴突
神经肽
医学
阿格里坎
作者
Xiaona Feng,Kaiwen Zhang,Techameena Prach,Rolen M. Quadros,Csaba Ádori,А. Р. Муртазина,Igor I. Adameyko,Sofia Biagini,Ozun Gokce Bayramlik,François Lallemend,Channabasavaiah B. Gurumurthy,Saïda Hadjab
标识
DOI:10.1038/s41467-026-70365-8
摘要
The regulation of nociceptor identity and function is essential, as disruptions can significantly influence pain sensation, yet our understanding of the molecular mechanisms involved remains incomplete. In this study, we identified ribonuclease 4 (RNase4) as selectively expressed in the unmyelinated nociceptor lineage. Analysis of RNase4-deficient mice and single-cell transcriptomic data revealed a cell-autonomous role for RNase4 in regulating nociceptor function. Moreover, in a neuropathic pain model, RNase4 expression was upregulated in nociceptors during the pain and recovery phases, and its deletion altered mechanical sensation. Additionally, RNase4 exerted non-cell- autonomous effects on the myelin structural organization of adjacent myelinated axons. Together, these findings implicate RNase4 as a dual regulator of nociceptor biology and myelin integrity, revealing a molecular pathway for pain regulation and nerve repair.
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