Acne is a common inflammatory and hereditary skin disorder. Previous genome-wide association studies (GWAS) have confirmed that genetic factors play a crucial role in its pathogenesis, while persistent local inflammation contributes to its chronic and recurrent nature. Infection with Cutibacterium acnes, activation of Toll-like receptors and the NLRP3 inflammasome, as well as dysregulation of the IL-6/STAT3 and Notch signaling pathways, induce the release of inflammatory cytokines and activation of inflammatory responses. Together with genetic predisposition, these mechanisms participate in the core cellular and molecular processes underlying acne development. This review systematically summarizes and analyzes how inflammation, at the cellular, molecular, and genetic levels, mediates the actions of key inflammatory factors and signaling pathways involved in acne pathogenesis, aiming to provide new insights and theoretical foundations for its prevention and treatment.
Han et al. (Mon,) studied this question.