ArticleClinical, cosmetic and investigational dermatology2024
Identification of Hub Genes in Comorbidity of Psoriasis and Vitiligo Using Bioinformatics Analysis.
Article in Clinical, cosmetic and investigational dermatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Vitiligo Information Resource database v3.NPJ systems biology and applications · 2026Article
- AR and ITGAL: Key Mediators of Andrographis paniculata's Anti-Psoriatic Effects Revealed by Multi-Omics Analysis.Combinatorial chemistry & high throughput screening · 2026Article
- Metabolic anomalies in vitiligo: a new frontier for drug repurposing strategies.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Psoriasis and vitiligo are two common autoimmune skin diseases with increased risk of comorbidities, but the common molecular mechanism about the occurrence of these two diseases is still unknown. Objective: This study aimed to identify the combined genetic profiles and evaluate the potential mechanism underlying the occurrence of this complication. Methods: The Gene Expression Omnibus (GEO) database was used to obtain the gene expression profiles of psoriasis (GSE30999) and vitiligo (GSE75819), and common differentially expressed genes (DEGs) were identified using GEO2R. DEGs were analyzed using functional enrichment analysis, protein-protein interaction (PPI) network and module construction, hub gene identification, and co-expression analysis. And hub genes were identified using Cytoscape software, and the gene expression of hub genes were validated in psoriasis (GSE13355) and vitiligo (GSE65127) datasets and immunohistochemistry at the clinical sample. Results: A total of 164 common DEGs with the same trend (137 upregulated and 27 downregulated) were selected for subsequent analysis. Functional analysis emphasized the important roles of the cell cycle and mitotic cell division, cytoskeletal reorganization, and chromatin remodeling in the complications of these two diseases. Fourteen important hub genes were identified, including BUB1, CEP55, CDK1, TOP2A, CENPF, PBK, MELK, CCNB2, MAD2L1, NUSAP1, TTK, NEK2, CDKN3, and PTTG1. Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) may be an important immune checkpoint in the pathogenesis of the comorbidities. Conclusion: Our study identified hub genes and potential mechanisms underlying psoriasis and vitiligo complications. And we proposed a new spatio-temporal theory and the probable immune checkpoint for the pathogenesis of the comorbidity which may provide new ideas for the further research.
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