Cardiovascular diseases are the leading cause of death in industrialized nations worldwide. Of all deaths
resulting from cardiovascular diseases, 2% are caused by inflammatory heart disease; specifically, myocarditis.
The etiology causing myocarditis still remains unclear. Both infectious and non-infectious factors are capable of
triggering myocarditis. Acute myocarditis manifests itself in a variety of ways ranging from subclinical disease to
sudden heart failure, as well as the occurrence of chest pain, palpitations, and syncope. Myocarditis can lead to dilated
cardiomyopathy, this being the most frequent cause for heart transplantation. Since the underlying mechanism
and the pathways behind the disease initiation and progression still need to be elucidated, the need for mouse models
simulating the human disease is evident. Various mouse models are frequently used to study myocarditis. Inflammation
of the myocardium as a result of infectious agents can be investigated with a widely used animal model
where mice are infected with coxsackievirus B3. For autoimmune (non-viral) myocarditis, several mouse models
(including induction with myosin or troponin I) have been established to better understand the role of autoantibodies and their influence
on disease progression. With these different models, various phases of the disease can be investigated and these findings are used to develop
more specific therapies that can be translated into the clinic as a "bench-to-bedside" approach.
Keywords: Animal models, myocarditis, autoimmunity, coxsackievirus B3, myosin, troponin I, DCM.
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