ArticlePLoS pathogens2014
Coxsackievirus-induced miR-21 disrupts cardiomyocyte interactions via the downregulation of intercalated disk components.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 51 citations in OpenAlex.
- Cyclodextrin Counteracts Coxsackievirus-Induced Cardiac Damage by Protecting Desmosome Integrity and Suppressing Proinflammatory Cytokine Expression.Microorganisms · 2025Article
- Heart-specific NFAT5 knockout suppresses type I interferon signaling and aggravates coxsackievirus-induced myocarditis.Basic research in cardiology · 2024Article
- The dual actions of miRNA16a in restricting Bovine Coronavirus replication through downregulation of Furin and enhancing the host immune response.Scientific reports · 2024Article
- Coxsackievirus B3-Induced mMicroorganisms · 2024Article
- The role of deubiquitinases in cardiac disease.Expert reviews in molecular medicine · 2024Review
- Crosstalk between ubiquitin ligases and ncRNAs drives cardiovascular disease progression.Frontiers in immunology · 2024Review
- Role of protein Post-translational modifications in enterovirus infection.Frontiers in microbiology · 2024Review
- MicroRNA expression profile of human umbilical vein endothelial cells in response to coxsackievirus A10 infection reveals a potential role of miR-143-3p in maintaining the integrity of the blood-brain barrier.Frontiers in cellular and infection microbiology · 2023Article
- Micro-Players of Great Significance-Host microRNA Signature in Viral Infections in Humans and Animals.International journal of molecular sciences · 2022Review
- The role of miRNAs in viral myocarditis, and its possible implication in induction of mRNA-based COVID-19 vaccines-induced myocarditis.Bulletin of the National Research Centre · 2022Review
- miRNAs: The Key Regulator of COVID-19 Disease.International journal of cell biology · 2022Review
- MicroRNA-324-3p Plays A Protective Role Against Coxsackievirus B3-Induced Viral Myocarditis.Virologica Sinica · 2021Article
- Breakdown of Filamentous Myofibrils by the UPS-Step by Step.Biomolecules · 2021Review
- Evaluation of MicroRNA-122 as a Biomarker for Chronic Hepatitis C Infection and as a Predictor for Treatment Response to Direct-Acting Antivirals.Hepatic medicine : evidence and research · 2021Article
- Regulatory RNAs in Heart Failure.Circulation · 2020Review
- Adrenergic Signaling-Induced Ultrastructural Strengthening of Intercalated Discs via Plakoglobin Is Crucial for Positive Adhesiotropy in Murine Cardiomyocytes.Frontiers in physiology · 2020Article
- Cleavage of Desmosomal Cadherins Promotes γ-Catenin Degradation and Benefits Wnt Signaling in Coxsackievirus B3-Induced Destruction of Cardiomyocytes.Frontiers in microbiology · 2020Article
- A novel circRNA-miRNA-mRNA network identifies circ-YOD1 as a biomarker for coronary artery disease.Scientific reports · 2019Article
- The protective role of microRNA-21 against coxsackievirus B3 infection through targeting the MAP2K3/P38 MAPK signaling pathway.Journal of translational medicine · 2019Article
- Glioblastoma-Associated Microglia Reprogramming Is Mediated by Functional Transfer of Extracellular miR-21.Cell reports · 2019Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Intercalated disks (ICDs) are substantial connections maintaining cardiac structures and mediating signal communications among cardiomyocytes. Deficiency in ICD components such as desmosomes, fascia adherens and gap junctions leads to heart dysfunction. Coxsackievirus B3 (CVB3) infection induces cardiac failure but its pathogenic effect on ICDs is unclear. Here we show that CVB3-induced miR-21 expression affects ICD structure, i.e., upregulated miR-21 targets YOD1, a deubiquitinating enzyme, to enhance the K48-linked ubiquitination and degradation of desmin, resulting in disruption of desmosomes. Inhibition of miR-21 preserves desmin during CVB3 infection. Treatment with proteasome inhibitors blocks miR-21-mediated desmin degradation. Transfection of miR-21 or knockdown of YOD1 triggers co-localization of desmin with proteasomes. We also identified K108 and K406 as important sites for desmin ubiquintination and degradation. In addition, miR-21 directly targets vinculin, leading to disturbed fascia adherens evidenced by the suppression and disorientation of pan-cadherin and α-E-catenin proteins, two fascia adherens-components. Our findings suggest a new mechanism of miR-21 in modulating cell-cell interactions of cardiomyocytes during CVB3 infection.
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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.