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氧化还原敏感的 Na/K-ATP 酶信号在尿毒症性心肌病中的作用。

The Redox-Sensitive Na/K-ATPase Signaling in Uremic Cardiomyopathy.

机构信息

Department of Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755, USA.

Department of Medicine, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25755, USA.

出版信息

Int J Mol Sci. 2020 Feb 13;21(4):1256. doi: 10.3390/ijms21041256.

Abstract

In recent years, Na/K-ATPase signaling has been implicated in different physiological and pathophysiological conditions, including cardiac hypertrophy and uremic cardiomyopathy. Cardiotonic steroids (CTS), specific ligands of Na/K-ATPase, regulate its enzymatic activity (at higher concentrations) and signaling function (at lower concentrations without significantly affecting its enzymatic activity) and increase reactive oxygen species (ROS) generation. On the other hand, an increase in ROS alone also regulates the Na/K-ATPase enzymatic activity and signaling function. We termed this phenomenon the Na/K-ATPase-mediated oxidant-amplification loop, in which oxidative stress regulates both the Na/K-ATPase activity and signaling. Most recently, we also demonstrated that this amplification loop is involved in the development of uremic cardiomyopathy. This review aims to evaluate the redox-sensitive Na/K-ATPase-mediated oxidant amplification loop and uremic cardiomyopathy.

摘要

近年来,Na/K-ATPase 信号转导与多种生理和病理生理状态有关,包括心肌肥厚和尿毒症性心肌病。强心甾类化合物(cardiotonic steroids,CTS)是 Na/K-ATPase 的特异性配体,可调节其酶活性(在较高浓度时)和信号功能(在较低浓度时,不显著影响其酶活性),并增加活性氧(reactive oxygen species,ROS)的产生。另一方面,ROS 的增加本身也可调节 Na/K-ATPase 的酶活性和信号功能。我们将这种现象称为 Na/K-ATPase 介导的氧化剂放大环,其中氧化应激调节 Na/K-ATPase 的活性和信号。最近,我们还证明了这种放大环参与了尿毒症性心肌病的发生发展。本文旨在评估氧化还原敏感的 Na/K-ATPase 介导的氧化剂放大环与尿毒症性心肌病的关系。

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