ArticleJournal of molecular and cellular cardiology2017
Spontaneous activation of a MAVS-dependent antiviral signaling pathway determines high basal interferon-β expression in cardiac myocytes.
Article in Journal of molecular and cellular cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- Reovirus µ2 residue 208 drives SRSF2-dependent nuclear hyperaccumulation of IRF9.microPublication biology · 2026Article
- Comparative analysis of the impact of interferon regulatory factors on basal and induced interferon and interferon stimulated gene expression in human and canine keratinocytes.Frontiers in immunology · 2026Article
- Old dogs-new tricks: multifaceted functions of MAVS beyond antivirus activity in human health and diseases.Cell & bioscience · 2025Review
- ARID5A orchestrates cardiac aging and inflammation through MAVS mRNA stabilization.Nature cardiovascular research · 2025Article
- Exploring the role of mitochondrial antiviral signaling protein in cardiac diseases.Frontiers in immunology · 2025Review
- From mitochondria to heart: the role and challenges of mitochondrial antiviral signaling protein in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
- Three modes of viral adaption by the heart.Science advances · 2024Article
- Junctophilin-2 is a double-stranded RNA-binding protein that regulates cardiomyocyte-autonomous innate immune response.Biochemical and biophysical research communications · 2024Article
- Three Modes of Viral Adaption by the Heart.bioRxiv : the preprint server for biology · 2024Article
- Redox Activation of Mitochondrial DAMPs and the Metabolic Consequences for Development of Autoimmunity.Antioxidants & redox signaling · 2022Review
- Reduced Immunity Regulator MAVS Contributes to Non-Hypertrophic Cardiac Dysfunction by Disturbing Energy Metabolism and Mitochondrial Homeostasis.Frontiers in immunology · 2022Article
- Human cardiac fibroblasts produce pro-inflammatory cytokines upon TLRs and RLRs stimulation.Molecular and cellular biochemistry · 2021Article
- Cell type-specific roles of PAR1 in Coxsackievirus B3 infection.Scientific reports · 2021Article
- The multi-functional reovirus σ3 protein is a virulence factor that suppresses stress granule formation and is associated with myocardial injury.PLoS pathogens · 2021Article
- "Sensing Danger": A New Player in the Innate Immune Response During Cardiac Pressure Overload.Circulation · 2020Article
- The RNA binding protein Quaking represses host interferon response by downregulating MAVS.RNA biology · 2020Article
- Efraín E. Rivera-Serrano: Personal training for scientists.The Journal of cell biology · 2019Article
- Biphasic and cardiomyocyte-specific IFIT activity protects cardiomyocytes from enteroviral infection.PLoS pathogens · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Viral myocarditis is a leading cause of sudden death in young adults as the limited turnover of cardiac myocytes renders the heart particularly vulnerable to viral damage. Viruses induce an antiviral type I interferon (IFN-α/β) response in essentially all cell types, providing an immediate innate protection. Cardiac myocytes express high basal levels of IFN-β to help pre-arm them against viral infections, however the mechanism underlying this expression remains unclear. Using primary cultures of murine cardiac and skeletal muscle cells, we demonstrate here that the mitochondrial antiviral signaling (MAVS) pathway is spontaneously activated in unstimulated cardiac myocytes but not cardiac fibroblasts or skeletal muscle cells. Results suggest that MAVS association with the mitochondrial-associated ER membranes (MAM) is a determinant of high basal IFN-β expression, and demonstrate that MAVS is essential for spontaneous high basal expression of IFN-β in cardiac myocytes and the heart. Together, results provide the first mechanism for spontaneous high expression of the antiviral cytokine IFN-β in a poorly replenished and essential cell type.
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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.