Renal Redox Balance and Na+, K+-ATPase Regulation: Role in Physiology and Pathophysiology

Silva, Elisabete; Soares‐da‐Silva, Patrício

doi:10.5772/34727

Cited by 4 publications

(3 citation statements)

References 95 publications

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“…In LLC-PK1 cells, ouabain-stimulated Na/K-ATPase signaling increases ROS generation. Other than ouabain, exogenous H 2 O 2 and glucose oxidase-induced H 2 O 2 also activate Na/K-ATPase signaling pathways including phosphorylation of c-Src and ERK1/2, as well as protein carbonylation modification of Na/K-ATPase (direct carbonylation of two amino acid residues, Pro 222 and Thr 224 , in the actuator domain of the α1 subunit) [84][85][86][87]. Pretreatment with antioxidant N-acetyl-l-cysteine (NAC) or disruption of the Na/K-ATPase/c-Src signaling complex attenuated ouabain-and glucose oxidase-stimulated Na/K-ATPase/c-Src signaling, protein carbonylation, redistribution of Na/K-ATPase, and inhibition of active transepithelial 22 Na + transport.…”

Section: The Na/k-atpase Signaling By Specific Ligands and Ros In Rptsmentioning

confidence: 99%

Section: Ros and The Na/k-atpase Signaling: The Possible Link From Ct...mentioning

confidence: 99%

“…In LLC-PK1 cells, both ouabain and glucose oxidase-induced H 2 O 2 stimulate Na/K-ATPase signaling as well as direct protein carbonylation of Pro 222 and Thr 224 residues of the Na/K-ATPase α1 subunit (α1-carbonylation) [86]. The Pro 222 and Thr 224 are located in peptide 211 VDNSSLTGESEPQTR 225 [UniProtKB/Swiss-Prot No P05024 (AT1A1_PIG)]. While the α1 subunit is highly conserved among humans, pigs, rats, and mice (the homology is over 98.5%), the identified peptide is 100% identical among these four species.…”

Section: Ros and The Na/k-atpase Signaling: The Possible Link From Ct...mentioning

confidence: 99%

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Biomarkers and Bioanalysis Overview

2021

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is a geneticist with a master's degree and Ph.D. in Medical Sciences and Nephrology from UFRGS/Brazil. She has postdoctoral experience in renal physiology (UFRJ/ Brazil), clinical medicine and nephrology (USP/Brazil), and nephrology and hypertension (UCI/USA). She is a Professor of Medical Genetics, Human Genetics, and Molecular Biology. Her research fields are human genetics diseases, cellular and molecular biology applied to nephrology, biochemistry, and microbiology with projects in the following subjects: inflammatory markers, molecular diagnosis, DNA polymorphisms, chronic kidney disease (CKD), polycystic kidney disease (PKD), Fabry disease, rare diseases, cellular and murine models for CKD, RNA processing, fluorescent image analysis, nanoparticles development, and nanomedicine.

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Section: The Na/k-atpase Signaling By Specific Ligands and Ros In Rptsmentioning

confidence: 99%

Section: Ros and The Na/k-atpase Signaling: The Possible Link From Ct...mentioning

confidence: 99%

Section: Ros and The Na/k-atpase Signaling: The Possible Link From Ct...mentioning

confidence: 99%

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Biomarkers and Bioanalysis Overview

2021

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Carbonylation Modification Regulates Na/K-ATPase Signaling and Salt Sensitivity: A Review and a Hypothesis

et al. 2016

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Na/K-ATPase signaling has been implicated in different physiological and pathophysiological conditions. Accumulating evidence indicates that oxidative stress not only regulates the Na/K-ATPase enzymatic activity, but also regulates its signaling and other functions. While cardiotonic steroids (CTS)-induced increase in reactive oxygen species (ROS) generation is an intermediate step in CTS-mediated Na/K-ATPase signaling, increase in ROS alone also stimulates Na/K-ATPase signaling. Based on literature and our observations, we hypothesize that ROS have biphasic effects on Na/K-ATPase signaling, transcellular sodium transport, and urinary sodium excretion. Oxidative modulation, in particular site specific carbonylation of the Na/K-ATPase α1 subunit, is a critical step in proximal tubular Na/K-ATPase signaling and decreased transcellular sodium transport leading to increases in urinary sodium excretion. However, once this system is overstimulated, the signaling, and associated changes in sodium excretion are blunted. This review aims to evaluate ROS-mediated carbonylation of the Na/K-ATPase, and its potential role in the regulation of pump signaling and sodium reabsorption in the renal proximal tubule (RPT).

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

Liu

Nie

Chaudhry

et al. 2020

IJMS

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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.

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Renal Redox Balance and Na+, K+-ATPase Regulation: Role in Physiology and Pathophysiology

Cited by 4 publications

References 95 publications

Biomarkers and Bioanalysis Overview

Biomarkers and Bioanalysis Overview

Carbonylation Modification Regulates Na/K-ATPase Signaling and Salt Sensitivity: A Review and a Hypothesis

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

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