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Related Concept Videos

Myocarditis I: Introduction01:21

Myocarditis I: Introduction

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Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
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Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

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Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
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Myocarditis III: Medical Management01:14

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Myocarditis: Comprehensive Medical ManagementMyocarditis, the heart muscle inflammation, requires a comprehensive medical management strategy that addresses the underlying cause, provides supportive care, manages symptoms, and reduces cardiac workload.Infections and Autoimmune CausesAdminister appropriate antimicrobial therapy when an infectious agent causes myocarditis. For instance, penicillin treats infections caused by Group A Streptococcus. In cases where autoimmune processes are...
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Cardiomyopathy II: Dilated Cardiomyopathy01:30

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Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
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Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

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Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
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Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
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Loeffler's Endomyocarditis: Clinical characteristics and outcomes from a tertiary care centre registry.

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Related Experiment Video

Updated: Feb 23, 2026

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TRAF6: A player in CVB3-induced myocarditis?

Oana N Ursu1, Tina Beyer1, Martina Sauter2

  • 1University Hospital Tübingen Medical Clinic, Department of Sports Medicine, Hoppe-Seyler-Str. 6, D-72076 Tübingen, Germany; University Hospital Tübingen, Department of Molecular Pathology, Institute for Pathology and Neuropathology, Liebermeisterstr. 8, D-72076 Tübingen, Germany.

Cytokine
|September 10, 2017
PubMed
Summary

Coxsackievirus B3 (CVB3) infection increases TNF receptor-associated factor 6 (TRAF6) levels in heart tissue and cells. However, TRAF6 induction is not essential for CVB3-induced nuclear factor kappa B (NFκB) activation.

Keywords:
CVB3HeLa cellsMyocarditisNFkappaBTRAF6

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Area of Science:

  • Virology
  • Immunology
  • Cardiology

Background:

  • Coxsackievirus B3 (CVB3) is a primary cause of myocarditis, potentially leading to dilated cardiomyopathy and heart failure.
  • The precise mechanisms underlying CVB3-induced heart disease chronification remain unclear.
  • TNF receptor-associated factor 6 (TRAF6) is a key signal transduction protein involved in immune responses downstream of cytokine receptors.

Purpose of the Study:

  • To investigate the role of TRAF6 gene expression in CVB3 infection.
  • To determine the relationship between TRAF6 levels and nuclear factor kappa B (NFκB) activation during CVB3 infection.
  • To analyze TRAF6's functional significance in CVB3-induced pathogenesis.

Main Methods:

  • Analysis of TRAF6 gene expression in heart tissue from susceptible and non-susceptible mouse strains post-CVB3 infection.
  • Assessment of TRAF6 levels and NFκB activity in CVB3-infected HeLa cells.
  • Functional analysis of TRAF6 using siRNA-mediated knockdown in HeLa cells.

Main Results:

  • TRAF6 expression was upregulated in CVB3-infected heart tissues of different mouse strains, with varying degrees of induction.
  • CVB3 infection moderately increased TRAF6 levels and strongly enhanced NFκB activity in HeLa cells.
  • Reduction of TRAF6 expression did not impact NFκB activation in response to CVB3 infection.

Conclusions:

  • CVB3 infection leads to increased TRAF6 expression in cardiac tissue and cells.
  • TRAF6 induction appears to be a consequence of CVB3 infection, but not a prerequisite for NFκB activation.
  • These findings suggest TRAF6 is not essential for the early NFκB-mediated response to CVB3 infection.