【摘要】 特应性皮炎(atopic dermatitis,AD)是一种以慢性瘙痒为特征性表现的炎症性皮肤病，其发病机制涉及神经、免疫与皮肤屏障之间复杂的交互作用。瞬时受体电位(transient receptor potential,TRP)通道作为多模态传感器，可被温度、炎症介质及机械刺激等多种因素激活。本综述系统阐释了TRP通道(包括TRPV1、TRPA1、TRPV3及TRPV4等)如何通过感知外源与内源刺激，调控痒觉信号传导、神经元敏化及神经源性炎症反应，促进AD瘙痒-搔抓恶性循环，在AD瘙痒的发生与维持中发挥核心作用。更多还原

【Abstract】 Atopic dermatitis( AD) is an inflammatory skin disorder characterized by chronic pruritus. Its pathogenesis involves complex interactions among the nervous system,immune system,and skin barrier. Transient receptor potential( TRP) channels,functioning as multimodal sensors that are activated by factors such as temperature,inflammatory mediators,and mechanical stimuli,play a pivotal role in the onset and maintenance of AD pruritus. This review systematically explains how TRP channels( including TRPV1,TRPA1,TRPV3,and TRPV4) regulate pruritus signaling,neuronal sensitization,and neurogenic inflammatory responses by sensing external and internal stimuli. This promotes the pruritus-scratch cycle in AD. This article objectively reviews recent advances in therapeutic strategies targeting TRP channels and provides the theoretical foundation for developing novel drugs to treat pruritus in AD.更多还原