The lipid–inflammation axis in rosacea: mechanistic insights and therapeutic implications

Rosacea is a chronic inflammatory skin disorder primarily characterized by persistent facial erythema, episodic flushing, papules and pustules, as well as phymatous changes. Despite extensive research, the pathogenesis of rosacea has not yet been fully elucidated. Current evidence suggests that rosacea develops on the basis of genetic susceptibility and results from the complex interplay of multiple endogenous and environmental factors, including immune dysregulation, impairment of skin barrier function, microbial imbalance, metabolic disturbances, and neurovascular dysfunction. Due to its chronic, refractory, and recurrent nature, rosacea imposes a substantial physical and psychological burden on affected individuals and markedly compromises quality of life. In recent years, accumulating studies have demonstrated that patients with rosacea frequently present with metabolic comorbidities related to lipid metabolism disorders, such as dyslipidemia, diabetes mellitus, and obesity. Notably, these metabolic abnormalities are reflected not only in circulating lipid profiles but also in alterations in the composition and proportion of facial sebum lipids. This review summarizes current evidence regarding abnormalities in serum lipid profiles and cutaneous lipid metabolism in patients with rosacea, and discusses the potential mechanisms by which dysregulated lipid metabolism may contribute to the initiation and progression of rosacea.