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首页> 外文期刊>Clinical & developmental immunology. >Cardiac Function Remains Impaired Despite Reversible Cardiac Remodeling after Acute Experimental Viral Myocarditis
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Cardiac Function Remains Impaired Despite Reversible Cardiac Remodeling after Acute Experimental Viral Myocarditis

机译:尽管急性实验性病毒性心肌炎后可逆性心脏重塑,心脏功能仍然受损

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摘要

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.
机译:背景 。柯萨奇病毒B3感染可诱发心肌炎。我们旨在比较病毒性心肌炎的急性和慢性阶段,以确定心脏炎症的即时影响以及解决炎症后对心脏纤维化进而对心脏功能的长期影响。材料与方法 。我们用柯萨奇病毒B3感染了C57BL / 6J小鼠,并在感染后7天和28天确定了其血流动力学功能。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纤维化信号。结果。在心肌炎的急性期,确定了严重的心脏炎症,并且心脏纤维化始终与炎症共存。感染后28天,心脏炎症反应下降,但血液动力学功能没有明显改善。有趣的是,心脏纤维化也下降至基础水平。在C57BL / 6J小鼠中,病毒性心肌炎治愈后,心脏炎症和纤维化都是可逆的,而血液动力学功能仍然受损。

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