ArticleJournal of multidisciplinary healthcare2025
Differential Expression of IFI16, IL-33 and CD55 Link Potential Common Pathogenic Mechanisms for COVID-19 and Ulcerative Colitis.
Article in Journal of multidisciplinary healthcare, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The Coronavirus disease 2019 (COVID-19) pandemic has significantly impacted global health and shares several clinical features with ulcerative colitis (UC). However, the existence of a common pathological mechanism between COVID-19 and UC remains uncertain. Additionally, effective treatment strategies for UC patients infected with COVID-19 are not well established. In this study, we investigate the potential shared pathogenesis of UC and COVID-19 and explore possible therapeutic regimens through bioinformatics and systems biology approaches. Methods: Common differentially expressed genes (DEGs) were extracted from the COVID-19 and ulcerative colitis (UC) datasets for functional enrichment, pathway analysis. The EnrichR database was used to predict potential transcription factors (TFs), microRNAs (miRNAs), and related drugs and diseases, enabling the construction of a regulatory network for both conditions. Results: We identified 115 significant common DEGs, with 11 high-confidence hub genes-including IFI16, IL-33, and CD55-implicated in innate immunity and inflammatory regulation. Pathway analysis revealed enrichment in interferon signaling, neutrophil activation, and cytokine-mediated responses. Regulatory network reconstruction highlighted miR-155-5p and transcription factors (eg, STAT1) as key regulators. Drug repurposing efforts prioritized retinoic acid, cyclosporine, and TD-139, which target these shared mechanisms. Conclusion: This study reveals robust molecular commonalities between COVID-19 and UC, highlighting dysregulated immune pathways and regulatory networks as shared mechanisms. We propose novel drug-repurposing candidates supported by network-based evidence, offering potential therapeutic strategies for patients with comorbid COVID-19 and UC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.