Evidence map›Paper›PMID 32587074›Full record

ArticleJournal of the American Society of Nephrology : JASN2020

Central Role for Adipocyte Na,K-ATPase Oxidant Amplification Loop in the Pathogenesis of Experimental Uremic Cardiomyopathy.

Komal Sodhi, Xiaoliang Wang, Muhammad Aslam Chaudhry, Hari Vishal Lakhani, Mishghan Zehra, Rebecca Pratt, Athar Nawab, Cameron L Cottrill, Brian Snoad, Fang Bai and 6 more

RetractedOpen access · bronzeAbstract readRetracted Publication
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
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  8. Observational
  9. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 2 institutions in 1 country.

Komal SodhiDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia.ORCID 0000-0002-1179-2985
Xiaoliang WangDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia.
Muhammad Aslam ChaudhryDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia.
Hari Vishal LakhaniDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia.
Mishghan ZehraDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia.
Rebecca PrattDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia.
Athar NawabDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia.
Cameron L CottrillDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia.
Brian SnoadDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia.
Fang BaiDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia.
James DenvirDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia.
Jiang LiuDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia.
Juan R SanabriaDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia.ORCID 0000-0002-7114-2327
Zijian XieDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia.
Nader G AbrahamDepartments of Medicine and Pharmacology, New York Medical College, Valhalla, New York.
Joseph I ShapiroDepartments of Medicine, Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia shapiroj@marshall.edu.
Marshall University · USNew York Medical College · US

Funding

West Virginia IDEA-CTRU54GM104942 · NIGMS · WEST VIRGINIA UNIVERSITY · PI Sally Lynn Hodder · 2012 to 2026
$81.0M
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
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
Role of Adipocyte Na/K-ATPase Signaling in the Development and Progression of Uremic Cardiomyopathy By Altering Adipocyte PhenotypeR15HL150721 · NHLBI · MARSHALL UNIVERSITY · PI SODHI, KOMAL · 2020 to 2020
$444k
The Role of Oxidative Signaling through Na/K-ATPase in Salt-Sensitive HypertensionR15DK106666 · NIDDK · MARSHALL UNIVERSITY · PI LIU, JIANG · 2016 to 2016
$435k
NHLBI NIH HHS P01 HL034300NHLBI NIH HHS R01 HL105649NHLBI NIH HHS R15 HL150721NHLBI NIH HHS U01 HL071556NIDDK NIH HHS R15 DK106666NIGMS NIH HHS U54 GM104942
6 · The paper itself

Abstract

backgroundOxidative stress in adipocyte plays a central role in the pathogenesis of obesity as well as in the associated cardiovascular complications. The putative uremic toxin indoxyl sulfate induces oxidative stress and dramatically alters adipocyte phenotype

methodsA lentivirus vector introduced the peptide NaKtide with an adiponectin promoter into the mouse model of experimental uremic cardiomyopathy, intraperitoneally. Then adipocyte-specific expression of the peptide was assessed for mice fed a standard diet compared with mice fed a western diet enriched in fat and fructose.

resultsPartial nephrectomy induced cardiomyopathy and anemia in the mice, introducing oxidant stress and an altered molecular phenotype of adipocytes that increased production of systemic inflammatory cytokines instead of accumulating lipids, within 4 weeks. Consumption of a western diet significantly worsened the adipocyte oxidant stress, but expression of NaKtide in adipocytes completely prevented the worsening. The peptide-carrying lentivirus achieved comparable expression in skeletal muscle, but did not ameliorate the disease phenotype.

conclusionsAdipocyte-specific expression of NaKtide, introduced with a lentiviral vector, significantly ameliorated adipocyte dysfunction and uremic cardiomyopathy in partially nephrectomized mice. These data suggest that the redox state of adipocytes controls the development of uremic cardiomyopathy in mice subjected to partial nephrectomy. If confirmed in humans, the oxidative state of adipocytes may be a therapeutic target in chronic renal failure.

Indexed as

AdipocytesAnimalsApoptosisCardiomyopathiesDisease Models, AnimalMaleMiceMice, Inbred C57BLNephrectomyOxidative StressPeptide FragmentsSodium-Potassium-Exchanging ATPaseUremiaNaKtidePeptide FragmentsSodium-Potassium-Exchanging ATPaseadipocytecardiovascular diseasechronic kidney diseaseobesityoxidative stressuremia

Identifiers

PMID32587074
PMCPMC7460907
OpenAlexW3037629554

What OpenQuestion holds

Textmetadata
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.