TY - CHAP
T1 - Viral Myocarditis and Dilated Cardiomyopathy
T2 - Mechanisms of Cardiac Injury, Inflammation, and Fibrosis
AU - Buskiewicz, Iwona
AU - Huber, Sally
AU - Fairweather, De Lisa
N1 - Funding Information:
This work was supported by the National Institute of Environmental Health Sciences and National Heart, Lung and Blood Institute of the National Institutes of Health Award Number R21 ES024414 and R01 HL111938, and an American Heart Association Grant-in-Aid 12GRNT12050000 to D.F.; HL108371 to S.H., I.B.; and in part from a grant from the Lupus Research Institute, Inc., and the National Center for Research Resources 5P20RR021905 and the National Institute of General Medical Sciences 8P20 GM103496 from the National Institutes of Health to I.B. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Publisher Copyright:
© 2016 Elsevier Inc. All rights reserved.
PY - 2016
Y1 - 2016
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
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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 -