ArticleMedComm2025
Loss of Adenosine Deaminase Acting on RNA 1 Induces Panoptosis and Immune Response in Ulcerative Colitis Gut Mucosa.
Article in MedComm, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Role of PANoptosis in the development of gastric immunity and related gastric mucosal disease (Review).Molecular medicine reports · 2026Review
- SMAD7-Associated Glycolytic Regulation Promotes Lactate-Dependent Macrophage Phenotype Modulation in Colorectal Cancer.Cancers · 2026Article
- BRD4 contributes to the cytokine-induced acquisition of an IL-13RA2-positive inflammatory fibroblast phenotype.Journal of Crohn's & colitis · 2026Article
- PANoptosis in the pathogenesis of myelodysplastic syndromes.Molecular oncology · 2026Review
- Role of PANoptosis in intestinal diseases and its therapeutic implications.Journal of molecular medicine (Berlin, Germany) · 2026Review
- The gut-heart dialogue: an epigenetic perspective on myocardial infarction.NPJ biofilms and microbiomes · 2026Review
- A multi-machine learning framework identifies novel PANoptosis-related biomarkers and their immune landscape in ulcerative colitis: Insights from transcriptomics and experimental validation.Frontiers in immunology · 2026Article
- PANoptosis: potential new targets and therapeutic prospects in digestive diseases.Apoptosis : an international journal on programmed cell death · 2025Review
- The role of ADAR1 in human pathophysiology.Frontiers in cell and developmental biology · 2025Review
- Zuoqing granules attenuate ulcerative colitis via macrophage polarization modulation: involvement of the PPAR-γ/NF-κB/STAT1 signaling axis.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The gut virome is a complex community that exists in equilibrium with the host. Disruptions of this balance could drive the development of inflammatory diseases, such as inflammatory bowel disease (IBD). RNA editing, particularly A-to-I editing by ADAR1, prevents the excessive immune response to viral double strand (ds) RNA. Failure of RNA editing may sustain inflammation and this study explore the role of ADAR1 in IBD. ADAR1 was analyzed in IBD patients and healthy controls (CTR) using western blotting and qPCR. Colonic epithelial cells (HCEC-1CT), ex vivo organ cultures, and colonic organoids were treated poly I:C after ADAR1 silencing with an antisense oligonucleotide (AS). Inflammatory pathways and PANoptosome were measured by western blotting, flow cytometry, and ELISA. The role of ADAR1 was also studied in DSS-colitis model. ADAR1 was significantly reduced in the inflamed epithelium of ulcerative colitis (UC) gut samples. ADAR1 silencing in HCEC-1CT, ex vivo organ cultures or colonic organoids strongly increases the immune response to poly I:C and leads to activation of inflammatory pathways and PANoptosis. Inhibition of gut ADAR1 expression during DSS-colitis exacerbated gut inflammation. JAK inhibition or AhR activation mitigated the immune response that follows ADAR1 silencing. These data suggest that ADAR1 could be involved in IBD inflammation.
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