Multiple studies have suggested that psoriasis may increase the risk of atrial fibrillation (AF). However, the molecular and immune mechanisms underlying this association remain unclear. This study initially downloaded gene expression profiles for psoriasis and AF from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) for both conditions were identified and hub genes were selected. Receiver operating characteristic (ROC) curve analysis and the prediction and validation of transcription factors (TFs) were conducted. Immune cell infiltration was analyzed using the CIBERSORT method. Mendelian randomization (MR) analysis was performed to explore the potential causal relationships between 731 Immunophenotypes and the risk of psoriasis and AF. A total of 1627 DEGs were identified from the psoriasis and AF datasets. Intersection analysis revealed 119 common DEGs. 10 potential biomarker hub genes, including GZMB, FCGR3B, LILRB2, IL7R, CD2, MYD88, NCF2, TLR2, GZMA, and CXCR2. ROC analysis showed that the area under the curve scores for the hub genes were 0.987 and 1.00 for psoriasis and AF, respectively. USF2, NFKB1 and RELA were predicted to be key TFs. Immune cell infiltration analysis indicated significant differences in T cell follicular helper, T cell gamma delta, and monocytes in the two diseases. MR analysis revealed 28 Immunophenotypes potentially associated with psoriasis risk and 18 traits potentially associated with AF risk. Notably, HLA DR + Natural Killer and CD39 on granulocyte cells were identified as influencing the risk of both diseases. This study preliminarily identified biomarkers and explored the molecular mechanisms of psoriasis and AF, highlighting immune cells potentially associated with disease pathogenesis. These findings provide a scientific basis for developing new diagnostic and therapeutic strategies, aiding in better prevention and management of AF risk in psoriasis patients.
Keywords: Atrial fibrillation; Biomarker; Immune infiltration; Mendelian randomization; Psoriasis.
© 2025. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.