Basic mechanisms in heart failure: the cytokine hypothesis.
Basic mechanisms in heart failure: the cytokine hypothesis.
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DOI：
10.1016/s1071-9164(96)80047-9
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发表时间：
1996-09-01
影响因子：
6
通讯作者：
Mann, D L
中科院分区：
文献类型：
--
作者：
Seta, Y;Shan, K;Mann, D L
虽然心力衰竭的发展和进展传统上被视为血液动力学紊乱，但现在越来越多的人意识到，心力衰竭综合征不能简单和/或精确地仅从血流动力学的角度来定义。所谓的血流动力学假说无法解释心力衰竭的进展，这引发了一种观念，即心力衰竭的进展可能是由于一系列生物活性分子过度表达的结果，这些分子通常被称为神经激素。最近，很明显，除了神经激素外，另一种被称为细胞因子的生物活性分子组合也在心力衰竭的环境中表达。本文综述了最近的临床和实验材料，认为细胞因子与神经激素非常相似，可能代表另一类生物活性分子，与心力衰竭的发生和发展有关。
Although the development and progression of heart failure have traditionally been viewed as hemodynamic disorders, there is now an increasing awareness that the syndrome of heart failure cannot be simply and/or precisely defined solely in hemodynamic terms. The inability of the so-called hemodynamic hypothesis to explain the progression of heart failure has given rise to the notion that heart failure may progress as a result of the overexpression of an ensemble of biologically active molecules referred to generically as neurohormones. More recently, it has become apparent that in addition to neurohormones, another portfolio of biologically active molecules, termed cytokines, are also expressed in the setting of heart failure. This article reviews recent clinical and experimental material that suggests that the cytokines, much like the neurohormones, may represent another class of biologically active molecules that are responsible for the development and progression of heart failure.