Evidence map›Paper›PMID 17517353›Full record

ArticleJournal of cardiac failure2007

Hypertrophy and heart failure in mice overexpressing the cardiac sodium-calcium exchanger.

Kenneth P Roos, Maria C Jordan, Michael C Fishbein, Matthew R Ritter, Martin Friedlander, Helen C Chang, Paymon Rahgozar, Tieyan Han, Alejandro J Garcia, W Robb Maclellan and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of cardiac failure, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

42 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
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  11. CaCell calcium · 2020
    Review
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  14. Review
  15. Article
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  18. Triggered activity in atrial myocytes is influenced by NaJournal of molecular and cellular cardiology · 2016
    Article
  19. Pivotal role of α2 NaThe Journal of physiology · 2016
    Review
  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

12 authors at 3 institutions in 1 country.

Kenneth P RoosDepartment of Physiology, The Cardiovascular Research Laboratory, David Geffen School of Medicine at UCLA, Los Angeles, California 90095-1751, USA.
Maria C Jordan
Michael C Fishbein
Matthew R Ritter
Martin Friedlander
Helen C Chang
Paymon Rahgozar
Tieyan Han
Alejandro J Garcia
W Robb Maclellan
Robert S Ross
Kenneth D Philipson
University of California, Los Angeles · USScripps Research Institute · USVA San Diego Healthcare System · US

Funding

Molecular Biology of Cardiac Sodium-Calcium ExchangeR01HL048509 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GOLDHABER, JOSHUA I, PHILIPSON, KENNETH · 2002 to 2016
$4.7M
MOLECULAR BIOLOGY OF CARDIAC SODIUM/CALCIUM EXCHANGER37HL048509 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PHILIPSON, KENNETH · 1992 to 2001
$702k
NHLBI NIH HHS HL-48509NHLBI NIH HHS R01 HL048509NHLBI NIH HHS R37 HL048509
6 · The paper itself

Abstract

backgroundThe cardiac sodium-calcium exchanger (NCX1) is a key sarcolemmal protein for the maintenance of calcium homeostasis in the heart. Because heart failure is associated with increased expression of NCX1, heterozygous (HET) and homozygous (HOM) transgenic mice overexpressing NCX1 were developed and evaluated. METHODS AND

resultsThe NCX1 transgenic mice display 2.3-fold (HET) and 3.1-fold (HOM) increases in exchanger activity from wild-type (WT) mice. Functional information was obtained by echocardiography and catheterizations before and after hemodynamic stress from pregnancy, treadmill exercise or transaortic constriction (TAC). HET and HOM mice exhibited hypertrophy and blunted responses with beta-adrenergic stimulation. Postpartum mice from all groups were hypertrophied, but only the HOM mice exhibited premature death from heart failure. HOM mice became exercise intolerant after 6 weeks of daily treadmill running. After 21 days TAC, HET, and HOM mice exhibited significant contractile dysfunction and 15% to 40% mortality with clinical evidence of heart failure.

conclusionsHemodynamic stress results in a compensated hypertrophy in WT mice, but NCX1 transgenic mice exhibit decreased contractile function and heart failure in proportion to their level of NCX1 expression. Thus exchanger overexpression in mice leads to abnormal calcium handling and a decompensatory transition to heart failure with stress.

Indexed as

Disease Models, AnimalAnimalsAnimals, Genetically ModifiedCardiomegalyFemaleGene ExpressionGene Expression ProfilingHeart FailureMaleMicePhenotypeSodium-Calcium ExchangerUltrasonographyNCX1 protein, mouseSodium-Calcium Exchanger

Identifiers

PMID17517353
PMCPMC2017112
OpenAlexW2146130130

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.