Targeting TRPV1 channels: new perspectives on the mechanisms of analgesia for herpes zoster neuralgia and advances in therapeutic research.

Herpes Zoster Neuralgia (HZN) is a condition caused by the varicella-zoster virus, characterized primarily by pain. The Transient Receptor Potential Vanilloid 1 (TRPV1), which acts as a pain mediator, plays a significant role in pain signaling and the regulation of neuroinflammation. In this context, this paper summarizes the biological characteristics of TRPV1, its dynamic expression in HZN, and its mechanisms for mediating neuroinflammatory processes and pain signal conduction. It posits that the inhibition of TRPV1 may alleviate HZN. Furthermore, the paper discusses the research and development progress, as well as the challenges associated with TRPV1 antagonists as a new class of analgesics, thereby providing new insights for the treatment of HZN.