ArticleNature communications2025
A loss-of-function human ADAR variant activates innate immune response and promotes bowel inflammation.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Review
- Article
- Targeting ADAR1 p150 triggers tumor inhibition and antitumor immunity to overcome immunotherapy resistance.iScience · 2026Article
- CVB-D attenuates experimental diabetic cardiomyopathy by alleviating mitochondrial dysfunction via the JAK1-STAT1 signaling axis in vivo and in vitro.Chinese medicine · 2026Article
- The gut-heart dialogue: an epigenetic perspective on myocardial infarction.NPJ biofilms and microbiomes · 2026Review
- From gut to pancreas: Shared genetic susceptibility and biological convergence in acute pancreatitis and Crohn's disease.PloS one · 2026Article
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Authors and funding
12 authors.
Funding
Abstract
Inflammatory bowel disease (IBD) arises from genetic-environmental interactions. Adenosine deaminases acting on RNA 1 (ADAR), an RNA-editing enzyme converting adenosine (A) to inosine (I), is essential for tissue homeostasis. Here we report that intestinal ADAR deficiency contributes to IBD pathogenesis in humans with reduced ADAR expression in patient intestinal crypts. Genetic or pharmacological inhibition of ADAR in mice causes spontaneous ileitis and colitis. Organoid studies show that ADAR loss leads to double-strand RNA (dsRNA) and endogenous retroviruses (ERVs) accumulation, disrupting intestinal homeostasis via melanoma differentiation-associated protein 5 (MDA5)-mediated dsRNA sensing and Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling. Editome analyses identify Mda5 as an ADAR target, and edited Mda5 exhibits impaired dsRNA sensing. The human ADAR p.N173S mutation is a loss-of-function variant that fails to rescue IBD in intestinal Adar deficient mice, whereas JAK1/2 inhibitor Ruxolitinib attenuates IBD. We conclude that the ADAR-dsRNA/ERVs-MDA5-JAK/STAT axis is a potential therapeutic target for IBD.
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