心肌炎
医学
扩张型心肌病
自身免疫
免疫学
心悸
心肌病
亚临床感染
疾病
病毒性心肌炎
柯萨奇病毒
心力衰竭
自身免疫性疾病
心脏病
内科学
心脏病学
病毒
免疫系统
肠道病毒
作者
Alexander Müller,Andrea Fischer,Hugo A. Katus,Ziya Kaya
标识
DOI:10.2174/1381612821666150316123711
摘要
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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