Role of SLC16A10 in Psoriasis Through the Regulation of Arachidonic Acid Metabolism in Keratinocytes

Abstract Psoriasis is an inflammatory dermatological condition challenging to treat and prone to recurrence. The pathogenesis of psoriasis is closely associated with metabolic disorders, while therapies targeting the dysregulated metabolism in psoriasis remain limited. Therefore, exploring the pathogenesis of psoriasis and identifying potential metabolic therapeutic targets is imperative. In this study, potential biomarkers for clinically targeted metabolic therapies in patients with psoriasis are aimed to be identified. RNA‐sequencing analysis is performed on metabolism‐related genes to identify differentially expressed metabolism‐related genes. Then, various bioinformatics analyses and comprehensive functional experiments are conducted to verify the roles of the identified genes. A key gene SLC16A10 is identified with significant diagnostic and therapeutic potential for psoriasis. SLC16A10 is likely involved in arachidonic acid metabolism in keratinocytes through regulating thyroid hormone homeostasis, contributing to the development of psoriasis. SLC16A10 represents a promising therapeutic target for guttate psoriasis and can improve the outcomes of existing immune‐targeted therapeutic agents. Comprehensive in vitro and in vivo experiments confirm that SLC16A10 downregulation alleviates the severity of psoriasis and hyperinflammation. Moreover, SLC16A10 may induce one of the sequelae of psoriasis, namely post‐inflammatory hypopigmentation, by inhibiting melanogenesis. These findings demonstrate the potential of SLC16A10 as a diagnostic biomarker and therapeutic target for psoriasis.