ArticlePloS one2024
Exploring the pathogenesis and immunological profiles of psoriasis complicated with MASLD.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Phenotypic Response Surfaces-Guided Optimization (PRS-OPT) of Propolis-Metformin-Regorafenib Combination Therapy for MASLD-Associated Hepatocellular Carcinoma.Oncology research · 2026Article
- Hidradenitis suppurativa and psoriasis: shared immunological links with metabolic-associated steatotic liver disease.Frontiers in immunology · 2026Review
- The Dual Role of IP-10/CXCL10 in Liver Injury: From Pathogenic Mediator to Clinical Biomarker and Therapeutic Target.Drug design, development and therapy · 2026Review
- Integrated bioinformatics and machine learning identify early diagnostic biomarkers for MAFLD with comorbid psoriasis.Frontiers in immunology · 2026Article
- Liver fibro-inflammation in psoriatic arthritis with MASLD improved by anti-IL-17 treatment: a clinical case.Rheumatology (Oxford, England) · 2025Article
- Up-regulated programmed cell death protein-1/its ligand 1 expression promotes metabolic dysfunction-associated steatotic liver disease malignant progression.World journal of gastrointestinal oncology · 2025Article
- Effect of Methotrexate Discontinuation on Psoriatic Patients with Significant Liver Fibrosis.Clinical, cosmetic and investigational dermatology · 2025Article
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundBoth psoriasis and metabolic dysfunction-associated steatotic liver disease (MASLD) are immune-mediated chronic inflammatory diseases. Psoriasis manifests itself mainly as skin damage, while MASLD mainly involves the liver promoting liver fibrosis, which has a significant impact on patient health and quality of life. Some clinical studies have shown that there are mutually reinforcing mechanisms between these two diseases, but they are not clearly defined, and this paper aims to further explore their common pathogenesis.
methodsGene expression profiling datasets (GSE30999, GSE48452) and single cell datasets (GSE151177, GSE186328) for psoriasis and MASLD were downloaded from the Gene Expression Omnibus (GEO) database. Common differential gene sets were obtained by gene differential analysis, and then functional enrichment of differential genes was performed to find associated transcription factors and PPI protein network analysis. Single-cell datasets were validated for gene expression and explored for cellular communication, gene set differential analysis and immune infiltration analysis.
resultsWe identified seven common differential genes, all of which were upregulated.The IL-17 pathway, tumor necrosis factor (TNF-α) pathway were shown in strong association with both diseases, and five transcription factors regulating the differential genes were predicted. Two key genes (MMP9, CXCL10) and three key transcription factors (TF) (IRF1, STAT1, NFKB1) were obtained by PPI protein network analysis. Single cell dataset verified the expression of key genes, and combined with gene set differential analysis, immune infiltration revealed that CD4+ T cells, NK cells and macrophages were heavily infiltrated in both diseases. IL-17, IL-1 and cGAS-STING pathways were highly expressed in both diseases, and both diseases share a similar immune microenvironment.
conclusionsOur study reveals the common pathogenesis of psoriasis and MASLD from gene expression to immune cell similarities and differences, identifies key genes and regulatory pathways common to both, and elucidates the similarities in the immune microenvironment of both diseases, providing new ideas for subsequent studies on targeted therapy.
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