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Cardiac Function Remains Impaired Despite Reversible Cardiac Remodeling after Acute Experimental Viral Myocarditis

Standard

Cardiac Function Remains Impaired Despite Reversible Cardiac Remodeling after Acute Experimental Viral Myocarditis. / Becher, Peter Moritz; Gotzhein, Frauke; Klingel, Karin; Escher, Felicitas; Blankenberg, Stefan; Westermann, Dirk; Lindner, Diana.

In: J IMMUNOL RES, 02.03.2017.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Becher, PM, Gotzhein, F, Klingel, K, Escher, F, Blankenberg, S, Westermann, D & Lindner, D 2017, 'Cardiac Function Remains Impaired Despite Reversible Cardiac Remodeling after Acute Experimental Viral Myocarditis', J IMMUNOL RES. https://doi.org/10.1155/2017/6590609

APA

Becher, P. M., Gotzhein, F., Klingel, K., Escher, F., Blankenberg, S., Westermann, D., & Lindner, D. (2017). Cardiac Function Remains Impaired Despite Reversible Cardiac Remodeling after Acute Experimental Viral Myocarditis. J IMMUNOL RES. https://doi.org/10.1155/2017/6590609

Vancouver

Becher PM, Gotzhein F, Klingel K, Escher F, Blankenberg S, Westermann D et al. Cardiac Function Remains Impaired Despite Reversible Cardiac Remodeling after Acute Experimental Viral Myocarditis. J IMMUNOL RES. 2017 Mar 2. https://doi.org/10.1155/2017/6590609

Bibtex

@article{28f3833a21984094b94f86bb7dd29292,
title = "Cardiac Function Remains Impaired Despite Reversible Cardiac Remodeling after Acute Experimental Viral Myocarditis",
abstract = "Background. Infection with Coxsackievirus B3 induces myocarditis. We aimed to compare the acute and chronic phases of viral myocarditis to identify the immediate effects of cardiac inflammation as well as the long-term effects after resolved inflammation on cardiac fibrosis and consequently on cardiac function. Material and Methods. We infected C57BL/6J mice with Coxsackievirus B3 and determined the hemodynamic function 7 as well as 28 days after infection. Subsequently, we analyzed viral burden and viral replication in the cardiac tissue as well as the expression of cytokines and matrix proteins. Furthermore, cardiac fibroblasts were infected with virus to investigate if viral infection alone induces profibrotic signaling. Results. Severe cardiac inflammation was determined and cardiac fibrosis was consistently colocalized with inflammation during the acute phase of myocarditis. Declined cardiac inflammation but no significantly improved hemodynamic function was observed 28 days after infection. Interestingly, cardiac fibrosis declined to basal levels as well. Both cardiac inflammation and fibrosis were reversible, whereas the hemodynamic function remains impaired after healed viral myocarditis in C57BL/6J mice.",
author = "Becher, {Peter Moritz} and Frauke Gotzhein and Karin Klingel and Felicitas Escher and Stefan Blankenberg and Dirk Westermann and Diana Lindner",
year = "2017",
month = mar,
day = "2",
doi = "10.1155/2017/6590609",
language = "English",
journal = "J IMMUNOL RES",
issn = "2314-8861",
publisher = "Hindawi Publishing Corporation",

}

RIS

TY - JOUR

T1 - Cardiac Function Remains Impaired Despite Reversible Cardiac Remodeling after Acute Experimental Viral Myocarditis

AU - Becher, Peter Moritz

AU - Gotzhein, Frauke

AU - Klingel, Karin

AU - Escher, Felicitas

AU - Blankenberg, Stefan

AU - Westermann, Dirk

AU - Lindner, Diana

PY - 2017/3/2

Y1 - 2017/3/2

N2 - Background. Infection with Coxsackievirus B3 induces myocarditis. We aimed to compare the acute and chronic phases of viral myocarditis to identify the immediate effects of cardiac inflammation as well as the long-term effects after resolved inflammation on cardiac fibrosis and consequently on cardiac function. Material and Methods. We infected C57BL/6J mice with Coxsackievirus B3 and determined the hemodynamic function 7 as well as 28 days after infection. Subsequently, we analyzed viral burden and viral replication in the cardiac tissue as well as the expression of cytokines and matrix proteins. Furthermore, cardiac fibroblasts were infected with virus to investigate if viral infection alone induces profibrotic signaling. Results. Severe cardiac inflammation was determined and cardiac fibrosis was consistently colocalized with inflammation during the acute phase of myocarditis. Declined cardiac inflammation but no significantly improved hemodynamic function was observed 28 days after infection. Interestingly, cardiac fibrosis declined to basal levels as well. Both cardiac inflammation and fibrosis were reversible, whereas the hemodynamic function remains impaired after healed viral myocarditis in C57BL/6J mice.

AB - Background. Infection with Coxsackievirus B3 induces myocarditis. We aimed to compare the acute and chronic phases of viral myocarditis to identify the immediate effects of cardiac inflammation as well as the long-term effects after resolved inflammation on cardiac fibrosis and consequently on cardiac function. Material and Methods. We infected C57BL/6J mice with Coxsackievirus B3 and determined the hemodynamic function 7 as well as 28 days after infection. Subsequently, we analyzed viral burden and viral replication in the cardiac tissue as well as the expression of cytokines and matrix proteins. Furthermore, cardiac fibroblasts were infected with virus to investigate if viral infection alone induces profibrotic signaling. Results. Severe cardiac inflammation was determined and cardiac fibrosis was consistently colocalized with inflammation during the acute phase of myocarditis. Declined cardiac inflammation but no significantly improved hemodynamic function was observed 28 days after infection. Interestingly, cardiac fibrosis declined to basal levels as well. Both cardiac inflammation and fibrosis were reversible, whereas the hemodynamic function remains impaired after healed viral myocarditis in C57BL/6J mice.

U2 - 10.1155/2017/6590609

DO - 10.1155/2017/6590609

M3 - SCORING: Journal article

C2 - 28352641

JO - J IMMUNOL RES

JF - J IMMUNOL RES

SN - 2314-8861

ER -