Involvement of Cytokines in the Pathogenesis of Salt and Water Imbalance in Congestive Heart Failure.
Involvement of Cytokines in the Pathogenesis of Salt and Water Imbalance in Congestive Heart Failure.
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DOI：
10.3389/fimmu.2017.00716
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发表时间：
2017
影响因子：
7.3
通讯作者：
Abassi Z
中科院分区：
文献类型：
--
作者：
Azzam ZS;Kinaneh S;Bahouth F;Ismael-Badarneh R;Khoury E;Abassi Z
充血性心力衰竭（CHF）已成为西方世界的主要医学问题，具有高发病率和死亡率。CHF对几个系统产生不利影响，主要是肾脏和肺。虽然在实验和临床CHF中，肾素-血管紧张素-醛固酮系统和交感神经系统参与心血管、肺和肾功能障碍的进展已得到充分证实，但促炎介质在该临床环境的发病机制中的重要性仍在不断发展。在这种情况下，CHF与促炎细胞因子的过度表达相关，如肿瘤坏死因子-α、白细胞介素（IL）-1和IL-6，这些细胞因子在环境损伤时被激活。该细胞因子家族与CHF的恶化有关，在心肌和循环水平启动和整合稳态应答中起重要作用。我们和其他研究人员发现，血管紧张素II通过促分裂原活化蛋白激酶p38和p42/44的磷酸化降低了肺清除水肿的能力，并增强了纤维化过程，这些蛋白激酶通常参与对促炎细胞因子的细胞反应。文献数据还表明这些效应物参与调节离子通道活性。据报告，在二尖瓣狭窄引起的心力衰竭中，存在不同程度的血管和其他相关实质变化，如水肿和纤维化。在这篇综述中，我们将讨论细胞因子和其他炎症介质对心力衰竭的肾脏和肺部的影响，特别是它们在肾脏和肺泡离子通道活性和液体平衡中的作用。
Congestive heart failure (CHF) has become a major medical problem in the western world with high morbidity and mortality rates. CHF adversely affects several systems, mainly the kidneys and the lungs. While the involvement of the renin–angiotensin–aldosterone system and the sympathetic nervous system in the progression of cardiovascular, pulmonary, and renal dysfunction in experimental and clinical CHF is well established, the importance of pro-inflammatory mediators in the pathogenesis of this clinical setting is still evolving. In this context, CHF is associated with overexpression of pro-inflammatory cytokines, such as tumor necrosis factor-α, interleukin (IL)-1, and IL-6, which are activated in response to environmental injury. This family of cytokines has been implicated in the deterioration of CHF, where it plays an important role in initiating and integrating homeostatic responses both at the myocardium and circulatory levels. We and others showed that angiotensin II decreased the ability of the lungs to clear edema and enhanced the fibrosis process via phosphorylation of the mitogen-activated protein kinases p38 and p42/44, which are generally involved in cellular responses to pro-inflammatory cytokines. Literature data also indicate the involvement of these effectors in modulating ion channel activity. It has been reported that in heart failure due to mitral stenosis; there were varying degrees of vascular and other associated parenchymal changes such as edema and fibrosis. In this review, we will discuss the effects of cytokines and other inflammatory mediators on the kidneys and the lungs in heart failure; especially their role in renal and alveolar ion channels activity and fluid balance.