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钠/氢交换体与心肌肥大

Na/H exchanger and cardiac hypertrophy.

作者信息

Yeves A M, Ennis I L

机构信息

Centro de Investigaciones Cardiovasculares "Horacio E. Cingolani", Facultad de Ciencias Médicas, Universidad Nacional de La Plata - CONICET, Calle 60 y 120, 1900 La Plata, Argentina.

Centro de Investigaciones Cardiovasculares "Horacio E. Cingolani", Facultad de Ciencias Médicas, Universidad Nacional de La Plata - CONICET, Calle 60 y 120, 1900 La Plata, Argentina.

出版信息

Hipertens Riesgo Vasc. 2020 Jan-Mar;37(1):22-32. doi: 10.1016/j.hipert.2019.09.002. Epub 2019 Oct 7.

DOI:10.1016/j.hipert.2019.09.002
PMID:31601481
Abstract

Reactive cardiac hypertrophy (CH) is an increase in heart mass in response to hemodynamic overload. Exercise-induced CH emerges as an adaptive response with improved cardiac function, in contrast to pathological CH that represents a risk factor for cardiovascular health. The Na/H exchanger (NHE-1) is a membrane transporter that not only regulates intracellular pH but also intracellular Na concentration. In the scenario of cardiovascular diseases, myocardial NHE-1 is activated by a variety of stimuli, such as neurohumoral factors and mechanical stress, leading to intracellular Na overload and activation of prohypertrophic cascades. NHE-1 hyperactivity is intimately linked to heart diseases, including ischemia-reperfusion injury, maladaptive CH and heart failure. In this review, we will present evidence to support that the NHE-1 hyperactivity constitutes a "switch on/off" for the pathological phenotype during CH development. We will also discuss some classical and novel strategies to avoid NHE-1 hyperactivity, and that are therefore worthwhile to improve cardiovascular health.

摘要

反应性心肌肥大(CH)是心脏质量因血流动力学负荷增加而增加。与代表心血管健康风险因素的病理性CH不同,运动诱导的CH是一种具有改善心脏功能的适应性反应。钠/氢交换体(NHE-1)是一种膜转运蛋白,不仅调节细胞内pH值,还调节细胞内钠浓度。在心血管疾病的情况下,心肌NHE-1被多种刺激激活,如神经体液因子和机械应力,导致细胞内钠过载和促肥大级联反应的激活。NHE-1活性过高与包括缺血再灌注损伤、适应性不良CH和心力衰竭在内的心脏病密切相关。在这篇综述中,我们将提供证据支持NHE-1活性过高在CH发展过程中构成病理性表型的“开关”。我们还将讨论一些避免NHE-1活性过高的经典和新策略,因此这些策略对于改善心血管健康是值得的。

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