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首页> 外文期刊>Journal of Cellular Physiology >Nongenomic signaling pathways triggered by thyroid hormones and their metabolite 3-iodothyronamine on the cardiovascular system.
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Nongenomic signaling pathways triggered by thyroid hormones and their metabolite 3-iodothyronamine on the cardiovascular system.

机译：Nongenomic信号通路引发的甲状腺激素及其代谢物3-iodothyronamine在心血管系统。

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摘要

Thyroid hormones play a wide range of important physiological activities in almost all organism. As changes in these hormones levels-observed in hypothyroidism and hyperthyroidism-promote serious derangements of the cardiovascular system, it is important to know their mechanisms of action. Although the classic genomic actions which are dependent on interaction with nuclear receptors to modulate cardiac myocytes genes expression, there is growing evidence about T(3) and T(4)-triggered nongenomic pathways, resulted from their binding to plasma membrane, cytoplasm, or mitocondrial receptors that leads to a rapidly regulation of cardiac functions. Interestingly both actions converge to amplify thyroid hormone effects on cardiovascular system. T(3) and T(4) nongenomic actions modify inotropic and chronotropic effects, cardiac action potential duration, cardiac growth, and myocyte shape by protein translation through protein kinases-dependent signaling cascades, which include PKA, PKC, PI3K, and MAPK, and changes on ion channels and pumps activity. In respect to the decreased systemic vascular resistance seen in hyperthyroidism, T(3) appears to activate NOS or ATP-sensitive K(+) channels. In addition, a novel biologically active T(4)-derived metabolite has been described, 3-iodothyronamine, T(1)AM, which also acts through membrane receptors to mediate nongenomic cardiac effects. This metabolite influences the physiological manifestations of thyroid hormone actions by inducing opposite effects from those stimulated by T(3) and T(4), such as negative inotropic and chronotropic effects. Therefore, beyond genomic and nongenomic effects of thyroid hormones, it is crucial for there to be an equilibrium between T(3) or T(4) and T(1)AM levels for maintaining cardiac homeostasis.
机译：甲状腺激素发挥广泛的重要在几乎所有生物体的生理活动。随着这些激素水平的变化甲状腺功能减退和hyperthyroidism-promote严重的心血管紊乱系统,重要的是要知道他们的机制的行动。哪些是依赖与核互动受体调节心脏细胞的基因表情,有越来越多的证据表明T (3)和T(4)——nongenomic通路,导致从他们的绑定到质膜、细胞质或mitocondrial受体导致迅速调节心脏功能。两个行动收敛于放大甲状腺激素对心血管系统的影响。修改变力和nongenomic行动变时性的影响,心脏动作电位持续时间、心脏增长,肌细胞的形状蛋白质翻译通过kinases-dependent信号级联,包括PKA、PKC PI3K和MAPK和变化离子通道和泵的活动。降低全身血管阻力在甲状腺机能亢进,T(3)似乎激活号或者ATP-sensitive K(+)通道。新型生物活性T(4)派生的代谢物被描述,3-iodothyronamine, T (1),通过膜受体作用调解nongenomic心脏的影响。代谢物的生理影响甲状腺激素的行为表现从这些刺激导致相反的效果T(3)和(4),如负性肌力和变时性的影响。和nongenomic甲状腺激素的影响,它是之间有一个平衡的关键T(3)和(4)和T(1)是维护水平心脏内稳态。

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