心力衰竭中的肿瘤坏死因子-α：更新综述。
Tumor Necrosis Factor-α in Heart Failure: an Updated Review.
机构信息
NB50, Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH, 44195, USA.
出版信息
Curr Cardiol Rep. 2018 Sep 26;20(11):117. doi: 10.1007/s11886-018-1067-7.
PURPOSE OF THE REVIEW
Proinflammatory cytokines are consistently elevated in congestive heart failure. In the current review, we provide an overview on the current understanding of how tumor necrosis factor-α (TNFα), a key proinflammatory cytokine, potentiates heart failure by overwhelming the anti-inflammatory responses disrupting the homeostasis.
RECENT FINDINGS
Studies have shown co-relationship between severity of heart failure and levels of the proinflammatory cytokine TNFα and one of its secondary mediators interleukin-6 (IL-6), suggesting their potential as biomarkers. Recent efforts have focused on understanding the mechanisms of how proinflammatory cytokines contribute towards cardiac dysfunction and failure. In addition, how unchecked proinflammatory cytokines and their cross-talk with sympathetic system overrides the anti-inflammatory response underlying failure. The review offers insights on how TNFα and IL-6 contribute to cardiac dysfunction and failure. Furthermore, this provides a forum to begin the discussion on the cross-talk between sympathetic drive and proinflammatory cytokines and its determinant role in deleterious outcomes.
目的综述
在充血性心力衰竭中，促炎细胞因子持续升高。在目前的综述中，我们概述了目前对肿瘤坏死因子-α（TNFα）（一种关键的促炎细胞因子）如何通过过度抑制抗炎反应破坏体内平衡从而加剧心力衰竭的理解。
最新发现
研究表明，心力衰竭的严重程度与促炎细胞因子 TNFα及其次级介质白细胞介素-6（IL-6）的水平之间存在相关性，这表明它们具有作为生物标志物的潜力。最近的研究重点是了解促炎细胞因子如何导致心脏功能障碍和衰竭的机制。此外，不受控制的促炎细胞因子及其与交感神经系统的相互作用如何超过失败的抗炎反应。该综述提供了关于 TNFα 和 IL-6 如何导致心脏功能障碍和衰竭的见解。此外，这为讨论交感神经驱动与促炎细胞因子之间的相互作用及其在有害后果中的决定作用提供了一个平台。
Zotero 插件