ACSL5 mediates macrophage infiltration and lipid metabolism in erythrotelangiectasia rosacea via potential pathogenic mechanisms and therapeutic targets.

Rosacea, an inflammatory skin disorder with complex pathogenesis, remains poorly understood. Through integrative bioinformatics and experimental approaches, we identified 304 differentially expressed genes in erythrotelangiectasia rosacea (ETR), primarily enriched in lipid metabolism pathways. Support vector machine (SVM), linear regression analyses and network analysis revealed ACADVL and ACSL5 as potential therapeutic targets. Immunological profiling demonstrated distinctive immune cell infiltration, with elevated M0 and M1 macrophages in patients with ETR. Immunofluorescence validation confirmed significant ACSL5 upregulation and increased M1 macrophage infiltration in the rosacea mouse model. The co-localization of ACSL5 with M1 macrophage markers suggests a mechanistic link between lipid metabolism and inflammatory responses. These findings provide new insights into ETR pathogenesis and highlight ACSL5 as a promising therapeutic target for inflammatory skin disorders.