ArticleScientific reports2023
Biomarkers of ulcerative colitis disease activity CXCL1, CYP2R1, LPCAT1, and NEU4 and their relationship to immune infiltrates.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Inflammatory and Immune Cytoprofiles of Active Ulcerative Colitis from Crohn's Disease-Insights from Multivariable Modeling.International journal of molecular sciences · 2026Article
- Protective Effect of Apiaceous Vegetables against Total Western Diet- and Dextran Sulfate Sodium-Induced Colitis in Mice.The Journal of nutrition · 2026Article
- Pharmacogenomic Pathways Underlying Variable Vedolizumab Response in Crohn's Disease Patients: A Rare-Variant Analysis.Biomedicines · 2026Article
- Deletion of Circadian Rhythms Gene BMAL1 Impairs the Intestinal Epithelial Barrier and Exacerbates Intestinal Inflammation by Inducing Pyroptosis.Mediators of inflammation · 2026Article
- The Gut Microbiota Affects Anti-TNF Responsiveness by Activating the NADAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Integrative machine learning and bioinformatics analysis to identify cellular senescence-related genes and potential therapeutic targets in ulcerative colitis and colorectal cancer.Frontiers in bioinformatics · 2025Article
- Identification of potential diagnostic markers and molecular mechanisms of asthma and ulcerative colitis based on bioinformatics and machine learning.Frontiers in molecular biosciences · 2025Article
- Article
- Identification and Validation of Feature Genes Related to Mitochondrial Dysfunction and Oxidative Stress in Ulcerative Colitis.Journal of inflammation research · 2025Article
- Interactions between NAD+ metabolism and immune cell infiltration in ulcerative colitis: subtype identification and development of novel diagnostic models.Frontiers in immunology · 2025Article
- The resolvin D2 and omega-3 polyunsaturated fatty acid as a new possible therapeutic approach for inflammatory bowel diseases.Scientific reports · 2024Article
- Unveiling and Validating the Role of Fatty Acid Metabolism in Ulcerative Colitis.Journal of inflammation research · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The diagnosis and assessment of ulcerative colitis (UC) poses significant challenges, which may result in inadequate treatment and a poor prognosis for patients. This study aims to identify potential activity biomarkers for UC and investigate the role of infiltrating immune cells in the disease. To perform gene set enrichment analysis, we utilized the cluster profiler and ggplot2 packages. Kyoto encyclopedia of genes and genomes was used to analyze degenerate enrichment genes. Significant gene set enrichment was determined using the cluster profiler and ggplot2 packages. Additionally, quantitative PCR (qRT-PCR) was employed to validate the expression of each marker in the ulcerative colitis model. We identified 651 differentially expressed genes (DEGs) and further investigated potential UC activity biomarkers. Our analysis revealed that CXCL1 (AUC = 0.710), CYP2R1 (AUC = 0.863), LPCAT1 (AUC = 0.783), and NEU4 (AUC = 0.833) were promising activity markers for the diagnosis of UC. Using rat DSS model, we validated these markers through qRT-PCR, which showed statistically significant differences between UC and normal colon mucosa. Infiltrating immune cell analysis indicated that M1 macrophages, M2 macrophages, activated dendritic cells (DCs), and neutrophils played crucial roles in the occurrence and progression of UC. Moreover, the activity markers exhibited varying degrees of correlation with activated memory CD4 T cells, M0 macrophages, T follicular helper cells, memory B cells, and activated DCs. The potential diagnostic genes for UC activity, such as CXCL1, CYP2R1, LPCAT1, and NEU4, as well as the infiltration of immune cells, may contribute to the pathogenesis and progression of UC.
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