RIPK3 promotes skin inflammation by enhancing IL-36α signaling and necroptosis in keratinocytes.

ABSTRACT: Psoriasis is a chronic inflammatory skin disease characterized by complex pathogenesis involving multiple factors. Keratinocytes, as key structural components, play a critical role in immune regulation and contribute to disease progression through interactions with various immune cells. Receptor-interacting protein kinase 3 (RIPK3) is well-known for its role in necroptosis, acting alongside RIPK1 and mixed-lineage kinase domain-like (MLKL). While studies have shown that inhibitors of necroptosis could alleviate psoriasis-like skin inflammation, direct genetic evidence of RIPK3 is lacking. Furthermore, recent studies have highlighted RIPK3's independent biological functions beyond necroptosis, yet its pathological role in inflammatory skin disease remains poorly understood. This study aimed

SUBMITTER: Li QQ 

PROVIDER: S-EPMC12552518 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature