The GH/IGF-1 Axis and Heart Failure
The GH/IGF-1 Axis and Heart Failure
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DOI：
10.2174/157340309788970306
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发表时间：
2009-01-01
影响因子：
1.9
通讯作者：
Fazio, Serafino
中科院分区：
文献类型：
--
作者：
Castellano, Graziella;Affuso, Flora;Fazio, Serafino
生长激素（GH）/胰岛素样生长因子1（IGF-1）轴调节心脏生长，刺激心肌收缩力并影响血管系统。GH/IGF-1轴通过增强细胞内钙的利用率和调节收缩蛋白的表达来控制固有的心脏收缩力;通过增加蛋白质合成来刺激心脏生长;通过激活一氧化氮系统和调节非内皮依赖性作用来改变全身血管阻力。GH/IGF-1轴与心血管系统之间的关系已在许多实验研究中得到广泛证实，并通过继发于GH过量和不足的心脏紊乱得到证实。几年前，一项临床非盲研究显示，在7例患有特发性扩张型心肌病和慢性心力衰竭（CHF）的患者中，使用重组GH加标准心力衰竭治疗3个月后，心脏功能和结构显著改善。最近的研究，包括一项关于GH对运动耐量和心肺功能影响的小型双盲安慰剂对照研究，表明GH对继发于缺血性和特发性扩张型心肌病的CHF患者有益。然而，其他安慰剂对照试验出现了相互矛盾的结果。这些不一致的发现可能是由CHF相关的GH耐药程度解释的。总之，我们认为，更多的临床和实验研究是必要的，以准确地了解的机制，确定变量的敏感性生长激素和其积极的影响，在衰竭的心脏。
The growth hormone (GH)/insulin-like growth factor 1 (IGF-1) axis regulates cardiac growth, stimulates myocardial contractility and influences the vascular system. The GH/IGF-1 axis controls intrinsic cardiac contractility by enhancing the intracellular calcium availability and regulating expression of contractile proteins; stimulates cardiac growth, by increasing protein synthesis; modifies systemic vascular resistance, by activating the nitric oxide system and regulating non-endothelial-dependent actions. The relationship between the GH/IGF-1 axis and the cardiovascular system has been extensively demonstrated in numerous experimental studies and confirmed by the cardiac derangements secondary to both GH excess and deficiency. Several years ago, a clinical non-blinded study showed, in seven patients with idiopathic dilated cardiomyopathy and chronic heart failure (CHF), a significant improvement in cardiac function and structure after three months of treatment with recombinant GH plus standard therapy for heart failure. More recent studies, including a small double-blind placebo-controlled study on GH effects on exercise tolerance and cardiopulmonary performance, have shown that GH benefits patients with CHF secondary to both ischemic and idiopathic dilated cardiomyopathy. However, conflicting results emerge from other placebo-controlled trials. These discordant findings may be explained by the degree of CHF-associated GH resistance. In conclusion, we believe that more clinical and experimental studies are necessary to exactly understand the mechanisms that determine the variable sensitivity to GH and its positive effects in the failing heart.