The Na,K-ATPase in vascular smooth muscle cells

Zhang, Lin; Staehr, Christian; Zeng, Fanxing; Bouzinova, Elena V.; Matchkov, Vladimir V.

doi:10.1016/bs.ctm.2019.01.007

Cited by 12 publications

(25 citation statements)

References 116 publications

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“…Several α and β isoforms, expressed in a tissue-specific manner, have been identified and functionally characterized (Blanco and Mercer 1998 ; Kaplan 2002 ; Sanchez et al 2006 ; Sweadner 1989 ). Since J.C. Skou's discovery in 1957 (Skou 1957 ), the energy-transducing Na/K-ATPase has been extensively studied for its ion pumping function and, later on, its signaling role (Aizman and Aperia 2003 ; Shapiro and Tian 2011 ; Xie and Cai 2003 ; Zhang et al 2019a ). Cardiotonic steroids (CTS, also known as digitalis-like substances) are specific Na/K-ATPase inhibitors and ligands.…”

Section: The Biology Of the Na/k-atpasementioning

confidence: 99%

“…Na/K-ATPase has been extensively studied for its ion transporting function since it was discovered in the 1950s. It was until the early 2000s, the signaling function of Na/K-ATPase started to be appreciated (Aizman and Aperia 2003 ; Shapiro and Tian 2011 ; Xie and Cai 2003 ; Zhang et al 2019a ).…”

Section: Mechanistic Perception Of Sglt2 Inhibitor and Na/k-atpasementioning

confidence: 99%

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The Na/K-ATPase Signaling and SGLT2 Inhibitor-Mediated Cardiorenal Protection: A Crossed Road?

et al. 2021

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In different large-scale clinic outcome trials, sodium (Na+)/glucose co-transporter 2 (SGLT2) inhibitors showed profound cardiac- and renal-protective effects, making them revolutionary treatments for heart failure and kidney disease. Different theories are proposed according to the emerging protective effects other than the original purpose of glucose-lowering in diabetic patients. As the ATP-dependent primary ion transporter providing the Na+ gradient to drive other Na+-dependent transporters, the possible role of the sodium–potassium adenosine triphosphatase (Na/K-ATPase) as the primary ion transporter and its signaling function is not explored. Graphic Abstract

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Section: The Biology Of the Na/k-atpasementioning

confidence: 99%

Section: Mechanistic Perception Of Sglt2 Inhibitor and Na/k-atpasementioning

confidence: 99%

The Na/K-ATPase Signaling and SGLT2 Inhibitor-Mediated Cardiorenal Protection: A Crossed Road?

et al. 2021

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“…In this regard, a reduction of the intracellular Ca 2+ -concentration has been reported to be due to the IP-induced preservation of Na + -K + -ATPase activity in the I/R hearts [ 52 ]. It should be mentioned that the Na + -K + -ATPase is considered to play a signaling function [ 130 , 131 , 132 , 133 , 134 ] and may act as a receptor transducing humoral signal [ 134 ]. Since ouabain activates several pathways that are involved in cardioprotection by IP, it has been suggested that protection against I/R injury by IP may involve the activation of the Na + -K + -ATPase/cSrc receptor complex and the subsequent stimulation of the key signaling mediators [ 135 , 136 ].…”

Section: Subcellular Modification Due To Ischemic Preconditioningmentioning

confidence: 99%

Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning

Tappia

Shah

Ramjiawan

et al. 2022

IJMS

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It is now well established that ischemia/reperfusion (I/R) injury is associated with the compromised recovery of cardiac contractile function. Such an adverse effect of I/R injury in the heart is attributed to the development of oxidative stress and intracellular Ca2+-overload, which are known to induce remodeling of subcellular organelles such as sarcolemma, sarcoplasmic reticulum, mitochondria and myofibrils. However, repeated episodes of brief periods of ischemia followed by reperfusion or ischemic preconditioning (IP) have been shown to improve cardiac function and exert cardioprotective actions against the adverse effects of prolonged I/R injury. This protective action of IP in attenuating myocardial damage and subcellular remodeling is likely to be due to marked reductions in the occurrence of oxidative stress and intracellular Ca2+-overload in cardiomyocytes. In addition, the beneficial actions of IP have been attributed to the depression of proteolytic activities and inflammatory levels of cytokines as well as the activation of the nuclear factor erythroid factor 2-mediated signal transduction pathway. Accordingly, this review is intended to describe some of the changes in subcellular organelles, which are induced in cardiomyocytes by I/R for the occurrence of oxidative stress and intracellular Ca2+-overload and highlight some of the mechanisms for explaining the cardioprotective effects of IP.

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“…ATP1 α 1 belongs to the Na + -K + ATPase subfamily and is regarded to be uniformly expressed in all cells [ 11 ]. As a muscle membrane pump, Na + -K + ATPase maintains a transmembrane Na + gradient, contributing to ion homeostasis [ 12 , 13 ]. It is known that the cardiac action potential is generated by the coordinated activation and inactivation of ion channels, which conduct depolarization (Na + and Ca 2+ ) currents and repolarization (K + ) currents [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Trimetazidine on Potassium Ion Homeostasis in Myocardial Tissue in Mice with Heart Failure

Yang

Yitao

et al. 2022

BioMed Research International

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The occurrence of heart failure (HF) is closely correlated with the disturbance of mitochondrial energy metabolism, and trimetazidine (TMZ) has been regarded as an effective agent in treating HF. Intracellular potassium ion (K+) homeostasis, which is modulated by K+ channels and transporters, is crucial for maintaining normal myocardial function and can be disrupted by HF. This study is aimed at exploring the protective effect of TMZ on K+ homeostasis within myocardial tissue in mice with HF. We observed the pathological changes of myocardial tissue under microscopes and further measured the content of adenosine triphosphate (ATP), the activity of Na+-K+ ATPase, and the expression of ATP1α1 at the mRNA and protein levels. Moreover, we also analyzed the changes in K+ flux across the myocardial tissue in mice. As a result, we found that there was a large amount of myocardial fiber lysis and fracture in HF myocardial tissue. Meanwhile, the potassium flux of mice with HF was reduced, and the expression of ATP1α1, the activity of Na+-K+ ATPase, and the supply and delivery of ATP were also decreased. In contrast, TMZ can effectively treat HF by restoring K+ homeostasis in the local microenvironment of myocardial tissues.

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The Na,K-ATPase in vascular smooth muscle cells

Cited by 12 publications

References 116 publications

The Na/K-ATPase Signaling and SGLT2 Inhibitor-Mediated Cardiorenal Protection: A Crossed Road?

The Na/K-ATPase Signaling and SGLT2 Inhibitor-Mediated Cardiorenal Protection: A Crossed Road?

Modification of Ischemia/Reperfusion-Induced Alterations in Subcellular Organelles by Ischemic Preconditioning

Protective Effect of Trimetazidine on Potassium Ion Homeostasis in Myocardial Tissue in Mice with Heart Failure

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