ArticleNature communications2024
ADAM9 promotes type I interferon-mediated innate immunity during encephalomyocarditis virus infection.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Antiviral innate immunity in myocarditis: mechanisms and emerging therapeutics.Experimental & molecular medicine · 2026Review
- ADAM9: an updated view of its biology and pathology.Molecular biology reports · 2026Review
- ADAM9 in tumor biology: molecular functions, clinical implications, and therapeutic targeting.Cellular & molecular biology letters · 2026Review
- RND3 restricts encephalomyocarditis virus replication by promoting IKKε ubiquitination and type I interferon production.Microbiology spectrum · 2026Article
- Zoological transmission of encephalomyocarditis virus in the United States: Virus evolution, host ecology, and capsid antigenicity derived from an outbreak.PLoS pathogens · 2026Article
- Multi-omics profiling identifies ADAM9 as a key efferocytosis driver in lung adenocarcinoma.Frontiers in immunology · 2026Article
- Ion channels and cardiac disease: mechanisms and functions of a disintegrin and metalloproteases and their substrates.Frontiers in cell and developmental biology · 2026Review
- Precision immunomodulation of viral myocarditis: a spatiotemporal intervention paradigm based on smart biomaterials.Frontiers in immunology · 2026Review
- Integrated Transcriptomic Analyses and Experimental Validation Identify TSPO as a Mitochondria-Associated Therapeutic Target in Myocarditis.Mediators of inflammation · 2026Article
- TRIM21 Exacerbates Ischemic Brain Injury by Promoting Astrocyte-Mediated Neuroinflammation via K63-Linked Ubiquitination of MDA5.Research (Washington, D.C.) · 2026Article
- The RIG-I-like receptor family of immune proteins.Molecular cell · 2025Review
- MDA5 ISGylation is crucial for immune signaling to control viral replication and pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- From mitochondria to heart: the role and challenges of mitochondrial antiviral signaling protein in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
- Exploring the role of mitochondrial antiviral signaling protein in cardiac diseases.Frontiers in immunology · 2025Review
- Therapeutic gene target prediction using novel deep hypergraph representation learning.Briefings in bioinformatics · 2024Article
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Authors and funding
18 authors.
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Abstract
Viral myocarditis, an inflammatory disease of the heart, causes significant morbidity and mortality. Type I interferon (IFN)-mediated antiviral responses protect against myocarditis, but the mechanisms are poorly understood. We previously identified A Disintegrin And Metalloproteinase domain 9 (ADAM9) as an important factor in viral pathogenesis. ADAM9 is implicated in a range of human diseases, including inflammatory diseases; however, its role in viral infection is unknown. Here, we demonstrate that mice lacking ADAM9 are more susceptible to encephalomyocarditis virus (EMCV)-induced death and fail to mount a characteristic type I IFN response. This defect in type I IFN induction is specific to positive-sense, single-stranded RNA (+ ssRNA) viruses and involves melanoma differentiation-associated protein 5 (MDA5)-a key receptor for +ssRNA viruses. Mechanistically, ADAM9 binds to MDA5 and promotes its oligomerization and thereby downstream mitochondrial antiviral-signaling protein (MAVS) activation in response to EMCV RNA stimulation. Our findings identify a role for ADAM9 in the innate antiviral response, specifically MDA5-mediated IFN production, which protects against virus-induced cardiac damage, and provide a potential therapeutic target for treatment of viral myocarditis.
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