Peng Shaoyi, Li Kaiyuan, Han Lingyu, Qiao Liang, Liu Peng
Department of Cardiology, The First People's Hospital of Jiande, Hangzhou, China.
Graduate School of Dalian Medical University, Dalian Medical University, Dalian, China.
Arch Dermatol Res. 2025 Jan 7;317(1):192. doi: 10.1007/s00403-024-03713-7.
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.
多项研究表明,银屑病可能会增加心房颤动(AF)的风险。然而,这种关联背后的分子和免疫机制仍不清楚。本研究最初从基因表达综合数据库下载了银屑病和心房颤动的基因表达谱。确定了两种疾病的差异表达基因(DEGs)并选择了枢纽基因。进行了受试者工作特征(ROC)曲线分析以及转录因子(TFs)的预测和验证。使用CIBERSORT方法分析免疫细胞浸润情况。进行孟德尔随机化(MR)分析以探索731种免疫表型与银屑病和心房颤动风险之间的潜在因果关系。从银屑病和心房颤动数据集中共鉴定出1627个DEGs。交叉分析揭示了119个共同的DEGs。10个潜在的生物标志物枢纽基因,包括颗粒酶B(GZMB)、Fc段γ受体Ⅲb(FCGR3B)、白细胞免疫球蛋白样受体B2(LILRB2)、白细胞介素7受体(IL7R)、分化簇2(CD2)、髓样分化因子88(MYD88)、中性粒细胞胞质因子2(NCF2)、Toll样受体2(TLR2)、颗粒酶A(GZMA)和CXC趋化因子受体2(CXCR2)。ROC分析表明,枢纽基因在银屑病和心房颤动中的曲线下面积得分分别为0.987和1.00。USF2、核因子κB1(NFKB1)和RelA被预测为关键转录因子。免疫细胞浸润分析表明,两种疾病中T滤泡辅助细胞、γδT细胞和单核细胞存在显著差异。MR分析揭示了28种可能与银屑病风险相关的免疫表型和18种可能与心房颤动风险相关的特征。值得注意的是,人类白细胞抗原DR(HLA DR)阳性自然杀伤细胞和粒细胞上的CD39被确定为影响两种疾病的风险。本研究初步确定了生物标志物并探索了银屑病和心房颤动的分子机制,突出了可能与疾病发病机制相关的免疫细胞。这些发现为制定新的诊断和治疗策略提供了科学依据,有助于更好地预防和管理银屑病患者的心房颤动风险。