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.

Key words: atopic dermatitis, pruritus, transient receptor potential