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
Affiliations
- Matthias Rohrbeck
- Institute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany
- Verena Hoerr
- Translational Research Imaging Center, Clinic of Radiology, University Hospital Münster, D-48149 Münster, Germany
- Ilaria Piccini
- Institute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany
- Boris Greber
- Human Stem Cell Pluripotency Laboratory, Max Planck Institute for Molecular Biomedicine, D-48149 Münster, Germany
- Jan Sebastian Schulte
- Institute of Pharmacology and Toxicology, University Hospital Münster, D-48149 Münster, Germany
- Sara-Sophie Hübner
- Translational Research Imaging Center, Clinic of Radiology, University Hospital Münster, D-48149 Münster, Germany
- Elena Jeworutzki
- Institute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany
- Carsten Theiss
- Department of Cytology, Institute of Anatomy, Ruhr-University Bochum, D-44780 Bochum, Germany
- Veronika Matschke
- Department of Cytology, Institute of Anatomy, Ruhr-University Bochum, D-44780 Bochum, Germany
- Jörg Stypmann
- Department of Cardiovascular Medicine, Division of Cardiology, University Clinic Münster, 48149 Münster, Germany
- Andreas Unger
- Institute of Physiology II, Faculty of Medicine, University of Münster, D-48149 Münster, Germany
- Huyen Tran Ho
- Institute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany
- Paul Disse
- Institute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany
- Nathalie Strutz-Seebohm
- Institute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany
- Cornelius Faber
- Translational Research Imaging Center, Clinic of Radiology, University Hospital Münster, D-48149 Münster, Germany
- Frank Ulrich Müller
- Institute of Pharmacology and Toxicology, University Hospital Münster, D-48149 Münster, Germany
- Stephan Ludwig
- Institute of Virology Münster (IVM), Centre for Molecular Biology of Inflammation (ZMBE), University of Münster, D-48149 Münster, Germany
- Ursula Rescher
- Research Group Regulatory Mechanisms of Inflammation, Institute of Medical Biochemistry, Centre for Molecular Biology of Inflammation, University of Muenster, 48149 Muenster, Germany
- Wolfgang A. Linke
- Institute of Physiology II, Faculty of Medicine, University of Münster, D-48149 Münster, Germany
- Karin Klingel
- Cardiopathology, Institute for Pathology and Neuropathology, University Hospital of Tübingen, D-72076 Tübingen, Germany
- Karin Busch
- Institute of Integrative Cell Biology and Physiology, Faculty of Biology, University of Muenster, Schlossplatz 5, 48149 Muenster, Germany
- Stefan Peischard
- Institute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany
- Guiscard Seebohm
- Institute for Genetics of Heart Diseases (IfGH), Department of Cardiovascular Medicine, University Hospital Münster, D-48149 Münster, Germany
- DOI
- https://doi.org/10.3390/cells12040550
- Journal volume & issue
-
Vol. 12,
no. 4
p. 550
Abstract
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.
Keywords