Various mouse models, including coxsackievirus B3 infection and induction with myosin or troponin I, are utilized to investigate the underlying mechanisms and progression of autoimmune myocarditis.
Mouse models of autoimmune myocarditis are essential for understanding disease mechanisms and developing targeted therapies for translation to the clinic.
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.
Müller et al. (Thu,) conducted a review in Autoimmune Myocarditis. Mouse models (coxsackievirus B3, myosin, troponin I) was evaluated. Various mouse models, including coxsackievirus B3 infection and induction with myosin or troponin I, are utilized to investigate the underlying mechanisms and progression of autoimmune myocarditis.
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