ArticleThe Journal of clinical investigation1998
Transgenic expression of replication-restricted enteroviral genomes in heart muscle induces defective excitation-contraction coupling and dilated cardiomyopathy.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 170 citations in OpenAlex.
- Increased expression of human endogenous retrovirus K in endomyocardial biopsies from patients with cardiomyopathy - a transcriptomics meta-analysis.BMC genomics · 2024Pooled it
- Dissecting myocardial and systemic drivers of cardiac dysfunction in the murine CVB3 myocarditis model using microRNA-guided viral detargeting.Basic research in cardiology · 2026Article
- Micro- and Nanoplastics as Potential Drivers of Dilated Cardiomyopathy.Life (Basel, Switzerland) · 2026Review
- Targeting Viperin prevents coxsackievirus B3-induced acute heart failure.Cell discovery · 2025Article
- Pathophysiological Mechanisms of Cardiac Dysfunction in Transgenic Mice with Viral Myocarditis.Cells · 2023Article
- Enterovirus-Cardiomyocyte Interactions: Impact of Terminally Deleted Genomic RNAs on Viral and Host Functions.Journal of virology · 2023Article
- Review
- SARS-CoV-2 Myocarditis: Insights Into Incidence, Prognosis, and Therapeutic Implications.Current cardiology reports · 2021Review
- Review
- Article
- Immunological and pathological consequences of coxsackievirus RNA persistence in the heart.Virology · 2017Article
- Persistent RNA virus infections: do PAMPS drive chronic disease?Current opinion in virology · 2017Review
- Cardiac Autoimmunity: Myocarditis.Advances in experimental medicine and biology · 2017Review
- Electrophysiological alterations in a murine model of chronic coxsackievirus B3 myocarditis.PloS one · 2017Article
- Structural interplay of KHeartRhythm case reports · 2016Article
- Major Persistent 5' Terminally Deleted Coxsackievirus B3 Populations in Human Endomyocardial Tissues.Emerging infectious diseases · 2016Article
- Recent progress in understanding coxsackievirus replication, dissemination, and pathogenesis.Virology · 2015Review
- c-FLIP-Short reduces type I interferon production and increases viremia with coxsackievirus B3.PloS one · 2014Article
- Viral myocarditis: from experimental models to molecular diagnosis in patients.Heart failure reviews · 2013Review
- Pharmacological and biological antiviral therapeutics for cardiac coxsackievirus infections.Molecules (Basel, Switzerland) · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Numerous studies have implicated Coxsackievirus in acute and chronic heart failure. Although enteroviral nucleic acids have been detected in selected patients with dilated cardiomyopathy, the significance of such persistent nucleic acids is unknown. To investigate the mechanisms by which restricted viral replication with low level expression of Coxsackieviral proteins may be able to induce cardiomyopathy, we generated transgenic mice which express a replication-restricted full-length Coxsackievirus B3 (CVB3) cDNA mutant (CVB3DeltaVP0) in the heart driven by the cardiac myocyte-specific myosin light chain-2v (MLC-2v) promoter. CVB3DeltaVP0 was generated by mutating infectious CVB3 cDNA at the VP4/VP2 autocatalytic cleavage site from Asn-Ser to Lys-Ala. Cardiac-specific expression of this cDNA leads to synthesis of positive- and negative-strand viral RNA in the heart without formation of infectious viral progeny. Histopathologic analysis of transgenic hearts revealed typical morphologic features of myocardial interstitial fibrosis and in some cases degeneration of myocytes, thus resembling dilated cardiomyopathy in humans. There was also an increase in ventricular atrial natriuretic factor mRNA levels, demonstrating activation of the embryonic program of gene expression typical of ventricular hypertrophy and failure. Echocardiographic analysis demonstrated the presence of left ventricular dilation and decreased systolic function in the transgenic mice compared with wild-type littermates, evidenced by increased ventricular end-diastolic and end-systolic dimensions and decreased fractional shortening. Analysis of isolated myocytes from transgenic mice demonstrate that there is defective excitation-contraction coupling and a decrease in the magnitude of isolated cell shortening. These data demonstrate that restricted replication of enteroviral genomes in the heart can induce dilated cardiomyopathy with excitation-contraction coupling abnormalities similar to pressure overload models of dilated cardiomyopathy.
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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.