Innate immunity and the failing heart: the cytokine hypothesis revisited.
Innate immunity and the failing heart: the cytokine hypothesis revisited.
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DOI：
10.1161/circresaha.116.302317
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发表时间：
2015-03-27
影响因子：
20.1
通讯作者：
Mann DL
中科院分区：
文献类型：
--
作者：
Mann DL
已在心力衰竭患者中确定炎性介质水平升高，包括射血分数降低和保留的心力衰竭以及急性失代偿性心力衰竭。此外，实验研究已经反复表明，心脏中炎症的激活引起左心室（LV）重构和LV功能障碍。尽管如此，试图拮抗炎症介质的III期临床试验在试验的主要终点方面呈阴性，并且在一些患者中导致心力衰竭恶化和/或死亡。以下综述将讨论先天免疫领域的最新进展如何促进我们对炎症在心力衰竭发病机制中的作用的理解，并将根据这些新信息讨论现有临床试验的负面结果。
Elevated levels of inflammatory mediators have been identified in patients with heart failure, including heart failure with reduced and preserved ejection fraction, as well as acute decompensated heart failure. Moreover, experimental studies have shown repeatedly that activation of inflammation in the heart provokes left ventricular (LV) remodeling and LV dysfunction. Nonetheless, phase III clinical trials that have attempted to antagonize inflammatory mediators have been negative with respect to the primary end points of the trials, and in some patients, resulted in worsening heart failure and/or death. The following review will discuss how recent developments in the field of innate immunity have advanced our understanding of the role of inflammation in the pathogenesis of heart failure and will discuss the negative outcomes of the existing clinical trials in light of this new information.