Cardiac Function Remains Impaired Despite Reversible Cardiac Remodeling after Acute Experimental Viral Myocarditis.
Cardiac Function Remains Impaired Despite Reversible Cardiac Remodeling after Acute Experimental Viral Myocarditis.
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DOI：
10.1155/2017/6590609
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发表时间：
2017
影响因子：
4.1
通讯作者：
Lindner D
中科院分区：
文献类型：
--
作者：
Becher PM;Gotzhein F;Klingel K;Escher F;Blankenberg S;Westermann D;Lindner D
背景。感染柯萨奇病毒 B3 会诱发心肌炎。我们的目的是比较病毒性心肌炎的急性期和慢性期，以确定心脏炎症的直接影响以及炎症消退后对心脏纤维化进而对心脏功能的长期影响。材料和方法。我们用柯萨奇病毒 B3 感染 C57BL/6J 小鼠，并在感染后 7 和 28 天测定血流动力学功能。随后，我们分析了心脏组织中的病毒负荷和病毒复制以及细胞因子和基质蛋白的表达。此外，心脏成纤维细胞被病毒感染，以研究病毒感染是否单独诱导促纤维化信号传导。结果。确定了严重的心脏炎症，并且在心肌炎的急性期期间，心脏纤维化始终与炎症共存。感染后 28 天观察到心脏炎症减少，但血流动力学功能没有明显改善。有趣的是，心脏纤维化也下降到基础水平。 C57BL/6J 小鼠的病毒性心肌炎治愈后，心脏炎症和纤维化都是可逆的，但血流动力学功能仍然受损。
Background. Infection with Coxsackievirus B3 induces myocarditis. We aimed to compare the acute and chronic phases of viral myocarditis to identify the immediate effects of cardiac inflammation as well as the long-term effects after resolved inflammation on cardiac fibrosis and consequently on cardiac function. Material and Methods. We infected C57BL/6J mice with Coxsackievirus B3 and determined the hemodynamic function 7 as well as 28 days after infection. Subsequently, we analyzed viral burden and viral replication in the cardiac tissue as well as the expression of cytokines and matrix proteins. Furthermore, cardiac fibroblasts were infected with virus to investigate if viral infection alone induces profibrotic signaling. Results. Severe cardiac inflammation was determined and cardiac fibrosis was consistently colocalized with inflammation during the acute phase of myocarditis. Declined cardiac inflammation but no significantly improved hemodynamic function was observed 28 days after infection. Interestingly, cardiac fibrosis declined to basal levels as well. Both cardiac inflammation and fibrosis were reversible, whereas the hemodynamic function remains impaired after healed viral myocarditis in C57BL/6J mice.