相关实验视频

Updated: Sep 15, 2025

Advanced Glycation End-Products Sensitize Human Sensory-Like Neuron Cells to Capsaicin-Induced Calcium Influx

Advanced Glycation End-Products Sensitize Human Sensory-Like Neuron Cells to Capsaicin-Induced Calcium Influx

Published on: May 2, 2025

感觉神经元表达的FGF13控制了糖尿病神经病变模型中的感觉信号

Aditya K Singh¹, Matteo Bernabucci¹, Nolan M Dvorak¹

¹Department of Pharmacology and Toxicology, The University of Texas Medical Branch, Galveston, Texas, USA.

The Journal of clinical investigation

|July 15, 2025

概括

纤维细胞生长因子13 (FGF13) 通过与Nav1.7.7相互作用,双向调节疼痛信号. 这种FGF13/Nav1.7复合体是糖尿病神经病痛的潜在治疗点.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
疼痛研究疼痛研究

背景情况:

nociception,有害刺激的信号传递,涉及复杂的途径.
双向调节 nociception 的内在机制尚未完全理解.
纤维细胞生长因子13 (FGF13) 和Nav1.7相互作用在疼痛中的作用尚未被探索.

研究的目的:

研究FGF13/Nav1.7蛋白与蛋白相互作用 (PPI) 综合体在调节恶感中的作用.
确定FGF13/Nav1.7比率是否在2型糖尿病神经病变 (T2DN) 中发生变化.
探索针对T2DN疼痛的FGF13/Nav1.7 PPI复合物的治疗潜力.

主要方法:

利用人类诱导的多能干细胞衍生 (hIPSC) 感觉神经元和小鼠模型.
研究了PPI抑制剂 (PW164) 和配体 (ZL192) 对离子电流和疼痛行为的影响.
检查了T2DN患者的背部根腺中的FGF13和Nav1.7同位体和比率.
分析了SCN9A变异对FGF13/Nav1.7 PPI的影响.

主要成果:

在FGF13/Nav1.7 PPI复合体双向调节 nociception.
PW164抑制了敏感的Na+电流和过敏症,而ZL192使电流敏感,并诱导了前感知行为.
在T2DN感觉神经元和患者中,FGF13/Nav1.7比率上调.
一种特定的SCN9A变种破坏了PW164对FGF13/Nav1.7 PPI的调节作用.

结论:

FGF13充当了可感觉的静脉静止剂.
FGF13/Nav1.7复合体是治疗2型糖尿病神经病变的疼痛管理的一个有希望的治疗点.
针对这种相互作用提供了局部疼痛缓解的潜力,系统副作用最小.

关键词:

神经科学是一个神经科学.疼痛疼痛疼痛疼痛公共卫生公共卫生通道中的.

更多相关视频

An Improved Assay and Tools for Measuring Mechanical Nociception in Drosophila Larvae

An Improved Assay and Tools for Measuring Mechanical Nociception in Drosophila Larvae

Published on: October 29, 2020

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1

Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1

Published on: February 13, 2018

相关概念视频

Nociception

Nociception

Nociception—the ability to feel pain—is essential for an organism’s survival and overall well-being. Noxious stimuli such as piercing pain from a sharp object, heat from an open flame, or contact with corrosive chemicals are first detected by sensory receptors, called nociceptors, located on nerve endings. Nociceptors express ion channels that convert noxious stimuli into electrical signals. When these signals reach the brain via sensory neurons, they are perceived as pain.