Cells (Feb 2023)

Pathophysiological Mechanisms of Cardiac Dysfunction in Transgenic Mice with Viral Myocarditis

  • Matthias Rohrbeck,
  • Verena Hoerr,
  • Ilaria Piccini,
  • Boris Greber,
  • Jan Sebastian Schulte,
  • Sara-Sophie Hübner,
  • Elena Jeworutzki,
  • Carsten Theiss,
  • Veronika Matschke,
  • Jörg Stypmann,
  • Andreas Unger,
  • Huyen Tran Ho,
  • Paul Disse,
  • Nathalie Strutz-Seebohm,
  • Cornelius Faber,
  • Frank Ulrich Müller,
  • Stephan Ludwig,
  • Ursula Rescher,
  • Wolfgang A. Linke,
  • Karin Klingel,
  • Karin Busch,
  • Stefan Peischard,
  • Guiscard Seebohm

DOI
https://doi.org/10.3390/cells12040550
Journal volume & issue
Vol. 12, no. 4
p. 550

Abstract

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Viral myocarditis is pathologically associated with RNA viruses such as coxsackievirus B3 (CVB3), or more recently, with SARS-CoV-2, but despite intensive research, clinically proven treatment is limited. Here, by use of a transgenic mouse strain (TG) containing a CVB3ΔVP0 genome we unravel virus-mediated cardiac pathophysiological processes in vivo and in vitro. Cardiac function, pathologic ECG alterations, calcium homeostasis, intracellular organization and gene expression were significantly altered in transgenic mice. A marked alteration of mitochondrial structure and gene expression indicates mitochondrial impairment potentially contributing to cardiac contractile dysfunction. An extended picture on viral myocarditis emerges that may help to develop new treatment strategies and to counter cardiac failure.

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