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Cardiology Research and Practice
Volume 2012 (2012), Article ID 437623, 11 pages
Research Article

Protective Function of STAT3 in CVB3-Induced Myocarditis

1Department of Cardiology and Pneumology, Charité-Universitäts-Medizin Berlin, Campus Benjamin Franklin, 12200 Berlin, Germany
2Department of Cardiology and Angiology, Hannover Medical School, 30625 Hannover, Germany
3Department of Molecular Pathology, University Hospital, 72076 Tübingen, Germany
4Department of Cardiology, Nuremberg Hospital South, 90471 Nürnberg, Germany

Received 6 February 2012; Accepted 13 March 2012

Academic Editor: Gregory Giamouzis

Copyright © 2012 Diana Lindner et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The transcription factor signal transducer and activator of transcription 3 (STAT3) is an important mediator of the inflammatory process. We investigated the role of STAT3 in viral myocarditis and its possible role in the development to dilated cardiomyopathy. We used STAT3-deficent mice with a cardiomyocyte-restricted knockout and induced a viral myocarditis using Coxsackievirus B3 (CVB3) which induced a severe inflammation during the acute phase of the viral myocarditis. A complete virus clearance and an attenuated inflammation were examined in both groups WT and STAT3 KO mice 4 weeks after infection, but the cardiac function in STAT3 KO mice was significantly decreased in contrast to the infected WT mice. Interestingly, an increased expression of collagen I was detected in STAT3 KO mice compared to WT mice 4 weeks after CVB3 infection. Furthermore, the matrix degradation was reduced in STAT3 KO mice which might be an explanation for the observed matrix deposition. Consequently, we here demonstrate the protective function of STAT3 in CVB3-induced myocarditis. Since the cardiomyocyte-restricted knockout leads to an increased fibrosis, it can be assumed that STAT3 signalling in cardiomyocytes protects the heart against increased fibrosis through paracrine effects.