ABSTRACT
This chapter introduces the modern concept of neurogenic inflammation as one of the possible neuronal mechanisms responsible for causing sensitive skin. The sensitive skin is related to altered somatosensory systems, especially lowered pain threshold and enhanced pain induction elicited by neurogenic inflammation and Transient receptor potential cation channel subfamily V member 1 (TRPV1) activation. It reviews the recognized roles of the vanilloid receptors, particularly TRPV1, in sensitive skin. The chapter summarizes that dysfunction of muscle contraction, carbohydrate and lipid metabolism, acidic homeostasis, and ion balance are important in the pathogenesis of sensitive skin. Further supporting experiments demonstrated that the decreased expressions of muscle-related genes in sensitive skin were not due to either a sampling bias or differences in anatomical sites. The treatment of rhabdomyosarcoma (RD) cells with Adiponectin, C1Q and collagen domain containing (ADIPOQ) induced a substantial reduction in the expressions of pain-related transcripts, suggesting a potential therapeutic role of ADIPOQ supplementation in sensitive skin.
