Evidence map›Paper›PMID 27698370›Full record

ArticleScientific reports2016

Attenuation of Na/K-ATPase Mediated Oxidant Amplification with pNaKtide Ameliorates Experimental Uremic Cardiomyopathy.

Jiang Liu, Jiang Tian, Muhammad Chaudhry, Kyle Maxwell, Yanling Yan, Xiaoliang Wang, Preeya T Shah, Asad A Khawaja, Rebecca Martin, Tylor J Robinette and 9 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
6.2field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 63 citations in OpenAlex.

  1. Na/K-ATPase Signaling in Adipocytes Promotes Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2026
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  10. NaExperimental biology and medicine (Maywood, N.J.) · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 3 institutions in 1 country.

Jiang LiuMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Jiang TianUniversity of Toledo, College of Medicine, 3000 Arlington Ave. Toledo, OH 43614 United States.
Muhammad ChaudhryMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Kyle MaxwellMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Yanling YanMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Xiaoliang WangMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Preeya T ShahMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Asad A KhawajaMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Rebecca MartinMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Tylor J RobinetteMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Adee El-HamdaniMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Michael W DodrillMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Komal SodhiMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Christopher A DrummondUniversity of Toledo, College of Medicine, 3000 Arlington Ave. Toledo, OH 43614 United States.
Steven T HallerUniversity of Toledo, College of Medicine, 3000 Arlington Ave. Toledo, OH 43614 United States.
David J KennedyUniversity of Toledo, College of Medicine, 3000 Arlington Ave. Toledo, OH 43614 United States.
Nader G AbrahamMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Zijian XieMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Joseph I ShapiroMarshall University, Joan C. Edwards School of Medicine, 1600 Medical Center Drive Huntington, 25701 United States.
Marshall University · USUniversity of Toledo · USNew York Medical College · US

Funding

Vasoregulatory Function of CYP2E1-Derived EicosanoidsP01HL034300 · NHLBI · NEW YORK MEDICAL COLLEGE · PI SCHWARTZMAN, MICHAL LANIADO · 1985 to 2015
$33.4M
CORAL: Clinical Coordinating CenterU01HL071556 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI COOPER, CHRISTOPHER J · 2004 to 2013
$19.3M
Receptor Na/K-ATPase Antagonists As Novel Therapeutics For Renal/Cardiac DiseasesR01HL109015 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI SHAPIRO, JOSEPH ISAAC, XIE, ZIJIAN · 2011 to 2014
$2.2M
Na/K-ATPase Reduction in Renal Disease-Related Cardiac DysfunctionR01HL105649 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI TIAN, JIANG · 2012 to 2016
$1.8M
The Role of Oxidative Signaling through Na/K-ATPase in Salt-Sensitive HypertensionR15DK106666 · NIDDK · MARSHALL UNIVERSITY · PI LIU, JIANG · 2016 to 2016
$435k
Evaluating the role of Exogenous administration of micro RNA 29b in preventing Chronic Kidney Disease induced cardiac FibrosisF32DK104615 · NIDDK · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI DRUMMOND, CHRISTOPHER ANSON · 2014 to 2016
$134k
American Heart Association-American Stroke Association 14SDG18650010NHLBI NIH HHS P01 HL034300NHLBI NIH HHS R01 HL105649NHLBI NIH HHS R01 HL109015NHLBI NIH HHS U01 HL071556NIDDK NIH HHS F32 DK104615NIDDK NIH HHS R15 DK106666
6 · The paper itself

Abstract

We have previously reported that the sodium potassium adenosine triphosphatase (Na/K-ATPase) can effect the amplification of reactive oxygen species. In this study, we examined whether attenuation of oxidant stress by antagonism of Na/K-ATPase oxidant amplification might ameliorate experimental uremic cardiomyopathy induced by partial nephrectomy (PNx). PNx induced the development of cardiac morphological and biochemical changes consistent with human uremic cardiomyopathy. Both inhibition of Na/K-ATPase oxidant amplification with pNaKtide and induction of heme oxygenase-1 (HO-1) with cobalt protoporphyrin (CoPP) markedly attenuated the development of phenotypical features of uremic cardiomyopathy. In a reversal study, administration of pNaKtide after the induction of uremic cardiomyopathy reversed many of the phenotypical features. Attenuation of Na/K-ATPase oxidant amplification may be a potential strategy for clinical therapy of this disorder.

Indexed as

AnimalsCardiomyopathiesDisease Models, AnimalEnzyme ActivatorsEnzyme InhibitorsHeme Oxygenase-1MaleMice, Inbred C57BLOxidantsProtoporphyrinsReactive Oxygen SpeciesSodium-Potassium-Exchanging ATPaseTreatment OutcomeUremiacobaltiprotoporphyrinEnzyme ActivatorsEnzyme InhibitorsHeme Oxygenase-1OxidantsProtoporphyrinsReactive Oxygen SpeciesSodium-Potassium-Exchanging ATPase

Identifiers

PMID27698370
PMCPMC5048179
OpenAlexW4236646947

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.