Background The association between psoriasis and cardiovascular disease (CVD) has long been discussed and continually refined. However, there is currently a lack of prospective studies on the cardiovascular risk attributed to psoriasis in the general population. Methods Representative adult participants were selected from the National Health and Nutrition Examination Survey (NHANES). Risks of cardiovascular symptoms and diseases prevalence were evaluated between participants with and without psoriasis. The hazards for all-cause mortality and CVD mortality were stratified by psoriasis status. Mediation analysis was then conducted to identify potential mediators between psoriasis and cardiac death. Results Overall, 19,741 participants were included in the current study, 542 (2.7%) had psoriasis and 19,199 (97.3%) did not have psoriasis. After adjusting for known CVD risk factors, odds for hypertension (OR = 1.37, 95% CI: 1.13-1.66, p= 0.001), hypercholesterolemia (OR = 1.37, 95% CI: 1.13-1.64, p < 0.001) and angina pectoris (OR = 1.74, 95% CI: 1.11-2.60, p = 0.011) were higher in psoriasis patients. Compared with participants without psoriasis, moderate/severe but not mild patients showed significantly higher CVD mortality (HR = 2.55, 95% CI: 1.27-5.15, p = 0.009). This result was supported by subgroup analyses. Mediation analysis further suggested that the direct effect of moderate/severe psoriasis on CVD mortality accounted for 81.4% (65.8%-97.1%). Besides, the indirect effect might derive from disturbance of serum albumin, urea nitrogen and uric acid. Conclusions Moderate-to-severe psoriasis is an independent risk factor for cardiovascular disease, making it necessary to regularly conduct cardiovascular disease-related examinations for patients with higher severity of psoriasis in clinical settings.

Chronic discoidal lupus erythematosus (CDLE) is an inflammatory skin disease characterized by localized, round, red, patchy skin lesions, which often occur on the head. Inflammatory cells often show an infiltration pattern targeting hair follicles, leading to alopecia. Our study aims to analyze the characteristics of gene expression data from hair follicle samples by bioinformatics methods, and the representative genes will be validated in data from skin samples with the same disease. The gene expression profile GSE119207 was obtained from the Gene Expression Omnibus (GEO) database as an experimental set, including microarray gene expression data of 4 healthy human hair follicles and 7 lesional and non-lesional hair follicles with CDLE. Gene profile GSE81071 included 13 healthy scalp samples and 47 scalp samples from CDLE lesions as the validation set. The experimental set was analyzed by differential gene expression analysis and WGCNA, respectively, and the intersection was taken to screen the key genes. The key genes were analyzed by GO and KEGG analysis to determine the related biological processes and pathways. The protein-protein interaction network of key genes was established by string and visualized by Cytoscape, and hub genes were obtained by cytoHubba. The acquired hub genes were used as ROC curve in the validation set to verify the consistency, and the related mirnas predicted by the hub genes were obtained by miRNet (version 2.0). Finally, cibersort was used to explore the infiltration pattern of immune cells in the hair follicles of CDLE. Through this process, we found that type I interferon response-related genes activated by the RIG-1 and IL-17 signaling pathways were significantly up-regulated, and the involved hub genes were also consistently upregulated in skin tissues. This process may involve the involvement of follicular helper T cells (Tfhs).

Chronic discoidal lupus erythematosus (CDLE) is an inflammatory skin disease characterized by localized, round, red, patchy skin lesions, which often occur on the head. Inflammatory cells often show an infiltration pattern targeting hair follicles, leading to alopecia. Our study aims to analyze the characteristics of gene expression data from hair follicle samples by bioinformatics methods, and the representative genes will be validated in data from skin samples with the same disease. The gene expression profile GSE119207 was obtained from the Gene Expression Omnibus (GEO) database as an experimental set, including microarray gene expression data of 4 healthy human hair follicles and 7 lesional and non-lesional hair follicles with CDLE. Gene profile GSE81071 included 13 healthy scalp samples and 47 scalp samples from CDLE lesions as the validation set. The experimental set was analyzed by differential gene expression analysis and WGCNA, respectively, and the intersection was taken to screen the key genes. The key genes were analyzed by GO and KEGG analysis to determine the related biological processes and pathways. The protein-protein interaction network of key genes was established by string and visualized by Cytoscape, and hub genes were obtained by cytoHubba. The acquired hub genes were used as ROC curve in the validation set to verify the consistency, and the related mirnas predicted by the hub genes were obtained by miRNet (version 2.0). Finally, cibersort was used to explore the infiltration pattern of immune cells in the hair follicles of CDLE. Through this process, we found that type I interferon response-related genes activated by the RIG-1 and IL-17 signaling pathways were significantly up-regulated, and the involved hub genes were also consistently upregulated in skin tissues. This process may involve the involvement of follicular helper T cells (Tfhs).