Viral Myocarditis and Dilated Cardiomyopathy: Mechanisms of Cardiac Injury, Inflammation, and Fibrosis

Iwona Buskiewicz, Sally Huber, DeLisa Fairweather

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Myocarditis is an inflammation of the myocardium, which often follows infection with one of many different pathogens including viruses, bacteria, protozoa, helminths, or fungi. Enteroviruses of the family of Picornaviruses (small, positive-sense, single-stranded RNA viruses) are a major etiological agent causing the clinical disease. Myocyte injury results from the direct infection and replication of the pathogen, from the innate and adaptive host immune responses to the infection, and from induction of autoimmunity to heart antigens. Chronic inflammation is likely due to autoimmunity, persistent viral infection in the heart, and an attempt to heal scar tissue laid down as a consequence of acute inflammation-induced remodeling. Profibrotic cytokines and mediators released during acute myocarditis in susceptible individuals activate fibroblasts and recruit new fibroblast differentiation via endothelial mesenchymal transition leading to cardiac remodeling and dilated cardiomyopathy.

Original languageEnglish (US)
Title of host publicationVascular Responses to Pathogens
PublisherElsevier Inc.
Pages149-159
Number of pages11
ISBN (Electronic)9780128013250
ISBN (Print)9780128010785
DOIs
StatePublished - Oct 27 2015
Externally publishedYes

Fingerprint

Myocarditis
Dilated Cardiomyopathy
Fibrosis
Inflammation
Autoimmunity
Wounds and Injuries
Fibroblasts
Infection
Picornaviridae
Enterovirus
Helminths
RNA Viruses
Adaptive Immunity
Virus Diseases
Muscle Cells
Cicatrix
Myocardium
Fungi
Cytokines
Viruses

Keywords

  • Coxsackievirus
  • Dilated cardiomyopathy
  • Endothelial mesenchymal transition
  • Fibrosis
  • Infection
  • Inflammation
  • Myocarditis

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Viral Myocarditis and Dilated Cardiomyopathy : Mechanisms of Cardiac Injury, Inflammation, and Fibrosis. / Buskiewicz, Iwona; Huber, Sally; Fairweather, DeLisa.

Vascular Responses to Pathogens. Elsevier Inc., 2015. p. 149-159.

Research output: Chapter in Book/Report/Conference proceedingChapter

Buskiewicz, Iwona ; Huber, Sally ; Fairweather, DeLisa. / Viral Myocarditis and Dilated Cardiomyopathy : Mechanisms of Cardiac Injury, Inflammation, and Fibrosis. Vascular Responses to Pathogens. Elsevier Inc., 2015. pp. 149-159
@inbook{5f6ee13ed5204ab49980923cfbeac983,
title = "Viral Myocarditis and Dilated Cardiomyopathy: Mechanisms of Cardiac Injury, Inflammation, and Fibrosis",
abstract = "Myocarditis is an inflammation of the myocardium, which often follows infection with one of many different pathogens including viruses, bacteria, protozoa, helminths, or fungi. Enteroviruses of the family of Picornaviruses (small, positive-sense, single-stranded RNA viruses) are a major etiological agent causing the clinical disease. Myocyte injury results from the direct infection and replication of the pathogen, from the innate and adaptive host immune responses to the infection, and from induction of autoimmunity to heart antigens. Chronic inflammation is likely due to autoimmunity, persistent viral infection in the heart, and an attempt to heal scar tissue laid down as a consequence of acute inflammation-induced remodeling. Profibrotic cytokines and mediators released during acute myocarditis in susceptible individuals activate fibroblasts and recruit new fibroblast differentiation via endothelial mesenchymal transition leading to cardiac remodeling and dilated cardiomyopathy.",
keywords = "Coxsackievirus, Dilated cardiomyopathy, Endothelial mesenchymal transition, Fibrosis, Infection, Inflammation, Myocarditis",
author = "Iwona Buskiewicz and Sally Huber and DeLisa Fairweather",
year = "2015",
month = "10",
day = "27",
doi = "10.1016/B978-0-12-801078-5.00012-1",
language = "English (US)",
isbn = "9780128010785",
pages = "149--159",
booktitle = "Vascular Responses to Pathogens",
publisher = "Elsevier Inc.",

}

TY - CHAP

T1 - Viral Myocarditis and Dilated Cardiomyopathy

T2 - Mechanisms of Cardiac Injury, Inflammation, and Fibrosis

AU - Buskiewicz, Iwona

AU - Huber, Sally

AU - Fairweather, DeLisa

PY - 2015/10/27

Y1 - 2015/10/27

N2 - Myocarditis is an inflammation of the myocardium, which often follows infection with one of many different pathogens including viruses, bacteria, protozoa, helminths, or fungi. Enteroviruses of the family of Picornaviruses (small, positive-sense, single-stranded RNA viruses) are a major etiological agent causing the clinical disease. Myocyte injury results from the direct infection and replication of the pathogen, from the innate and adaptive host immune responses to the infection, and from induction of autoimmunity to heart antigens. Chronic inflammation is likely due to autoimmunity, persistent viral infection in the heart, and an attempt to heal scar tissue laid down as a consequence of acute inflammation-induced remodeling. Profibrotic cytokines and mediators released during acute myocarditis in susceptible individuals activate fibroblasts and recruit new fibroblast differentiation via endothelial mesenchymal transition leading to cardiac remodeling and dilated cardiomyopathy.

AB - Myocarditis is an inflammation of the myocardium, which often follows infection with one of many different pathogens including viruses, bacteria, protozoa, helminths, or fungi. Enteroviruses of the family of Picornaviruses (small, positive-sense, single-stranded RNA viruses) are a major etiological agent causing the clinical disease. Myocyte injury results from the direct infection and replication of the pathogen, from the innate and adaptive host immune responses to the infection, and from induction of autoimmunity to heart antigens. Chronic inflammation is likely due to autoimmunity, persistent viral infection in the heart, and an attempt to heal scar tissue laid down as a consequence of acute inflammation-induced remodeling. Profibrotic cytokines and mediators released during acute myocarditis in susceptible individuals activate fibroblasts and recruit new fibroblast differentiation via endothelial mesenchymal transition leading to cardiac remodeling and dilated cardiomyopathy.

KW - Coxsackievirus

KW - Dilated cardiomyopathy

KW - Endothelial mesenchymal transition

KW - Fibrosis

KW - Infection

KW - Inflammation

KW - Myocarditis

UR - http://www.scopus.com/inward/record.url?scp=84980320239&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84980320239&partnerID=8YFLogxK

U2 - 10.1016/B978-0-12-801078-5.00012-1

DO - 10.1016/B978-0-12-801078-5.00012-1

M3 - Chapter

AN - SCOPUS:84980320239

SN - 9780128010785

SP - 149

EP - 159

BT - Vascular Responses to Pathogens

PB - Elsevier Inc.

ER -