Evidence map›Paper›PMID 28338377›Full record

ReviewExpert opinion on therapeutic targets2017

Sodium potassium adenosine triphosphatase (Na/K-ATPase) as a therapeutic target for uremic cardiomyopathy.

Xiaoliang Wang, Jiang Liu, Christopher A Drummond, Joseph I Shapiro

Open access · greenAbstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. The NaFrontiers in endocrinology · 2023
    Review
  4. Article
  5. NaExperimental biology and medicine (Maywood, N.J.) · 2022
    Article
  6. Review
  7. Dietary choline,Frontiers in physiology · 2022
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Xiaoliang Wanga Joan C Edwards School of Medicine at Marshall University , Huntington , WV , United States.
Jiang Liua Joan C Edwards School of Medicine at Marshall University , Huntington , WV , United States.
Christopher A Drummondb University of Toledo College of Medicine and Life Sciences , Toledo , OH , United States.
Joseph I Shapiroa Joan C Edwards School of Medicine at Marshall University , Huntington , WV , United States.
Marshall University · USUniversity of Toledo · US

Funding

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
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
NHLBI NIH HHS R01 HL105649NHLBI NIH HHS U01 HL071556NIDDK NIH HHS F32 DK104615NIDDK NIH HHS R15 DK106666
6 · The paper itself

Abstract

introductionClinically, patients with significant reductions in renal function present with cardiovascular dysfunction typically termed, uremic cardiomyopathy. It is a progressive series of cardiac pathophysiological changes, including left ventricular diastolic dysfunction and hypertrophy (LVH) which sometimes progress to left ventricular dilation (LVD) and systolic dysfunction in the setting of chronic kidney disease (CKD). Uremic cardiomyopathy is almost ubiquitous in patients afflicted with end stage renal disease (ESRD). Areas covered: This article reviews recent epidemiology, pathophysiology of uremic cardiomyopathy and provide a board overview of Na/K-ATPase research with detailed discussion on the mechanisms of Na/K-ATPase/Src/ROS amplification loop. We also present clinical and preclinical evidences as well as molecular mechanism of this amplification loop in the development of uremic cardiomyopathy. A potential therapeutic peptide that targets on this loop is discussed. Expert opinion: Current clinical treatment for uremic cardiomyopathy remains disappointing. Targeting the ROS amplification loop mediated by the Na/K-ATPase signaling function may provide a novel therapeutic target for uremic cardiomyopathy and related diseases. Additional studies of Na/K-ATPase and other strategies that regulate this loop will lead to new therapeutics.

Indexed as

AnimalsCardiomegalyCardiomyopathiesHumansKidney Failure, ChronicMolecular Targeted TherapyPeptidesReactive Oxygen SpeciesSodium-Potassium-Exchanging ATPaseUremiaVentricular Dysfunction, LeftPeptidesReactive Oxygen SpeciesSodium-Potassium-Exchanging ATPasecell signalingNa/K-ATPaseROSuremic cardiomyopathy

Identifiers

PMID28338377
PMCPMC5590225
OpenAlexW2599558286

What OpenQuestion holds

Textmetadata
LicenceTDM
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.