Evidence map›Paper›PMID 27667975›Full record

ReviewFrontiers in physiology2016

Regulation of Cardiac Remodeling by Cardiac Na(+)/K(+)-ATPase Isoforms.

Lijun Liu, Jian Wu, David J Kennedy

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 48 citations in OpenAlex.

  1. Phenotype-specific muscle proteomic profiling in titinopathies.Acta neuropathologica communications · 2026
    Article
  2. Review
  3. Article
  4. The NaFrontiers in endocrinology · 2023
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. The NaCellular and molecular life sciences : CMLS · 2021
    Review
  13. Article
  14. Review
  15. Proteomic Profiling Reveals Roles of Stress Response, CaAlcoholism, clinical and experimental research · 2020
    Article
  16. Article
  17. Review
  18. TBC1D25 Regulates Cardiac Remodeling Through TAK1 Signaling Pathway.International journal of biological sciences · 2020
    Article
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Lijun LiuDepartment of Medicine, College of Medicine and Life Sciences, University of Toledo Toledo, OH, USA.
Jian WuCenter for Craniofacial Molecular Biology, University of Southern California Los Angeles, CA, USA.
David J KennedyDepartment of Medicine, College of Medicine and Life Sciences, University of Toledo Toledo, OH, USA.
University of Toledo · USUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac remodeling occurs after cardiac pressure/volume overload or myocardial injury during the development of heart failure and is a determinant of heart failure. Preventing or reversing remodeling is a goal of heart failure therapy. Human cardiomyocyte Na(+)/K(+)-ATPase has multiple α isoforms (1-3). The expression of the α subunit of the Na(+)/K(+)-ATPase is often altered in hypertrophic and failing hearts. The mechanisms are unclear. There are limited data from human cardiomyocytes. Abundant evidences from rodents show that Na(+)/K(+)-ATPase regulates cardiac contractility, cell signaling, hypertrophy and fibrosis. The α1 isoform of the Na(+)/K(+)-ATPase is the ubiquitous isoform and possesses both pumping and signaling functions. The α2 isoform of the Na(+)/K(+)-ATPase regulates intracellular Ca(2+) signaling, contractility and pathological hypertrophy. The α3 isoform of the Na(+)/K(+)-ATPase may also be a target for cardiac hypertrophy. Restoration of cardiac Na(+)/K(+)-ATPase expression may be an effective approach for prevention of cardiac remodeling. In this article, we will overview: (1) the distribution and function of isoform specific Na(+)/K(+)-ATPase in the cardiomyocytes. (2) the role of cardiac Na(+)/K(+)-ATPase in the regulation of cell signaling, contractility, cardiac hypertrophy and fibrosis in vitro and in vivo. Selective targeting of cardiac Na(+)/K(+)-ATPase isoform may offer a new target for the prevention of cardiac remodeling.

Indexed as

cardiac remodelingcardiomyocytefibrosishypertrophyisoformNa+/K+-ATPaseouabain

Identifiers

PMID27667975
PMCPMC5016610
OpenAlexW2509440351

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.