Evidence map›Paper›PMID 23608603›Full record

ReviewJournal of molecular and cellular cardiology2013

Na⁺ transport in the normal and failing heart - remember the balance.

Sanda Despa, Donald M Bers

Abstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
–field-weighted citation impact
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

86 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  6. Article
  7. Regulation of Na/Ca exchange by cytoplasmic protons modifies intracellular calcium dynamics and the cardiac response to ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Review
  10. Article
  11. Role of NaInternational journal of molecular sciences · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Metabolic Approaches for the Treatment of Dilated Cardiomyopathy.Journal of cardiovascular development and disease · 2023
    Review
  19. Review
  20. Antiarrhythmic and Inotropic Effects of Selective NaInternational journal of molecular sciences · 2022
    Review

26 more citing papers are in PubMed but not listed here.

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

2 authors.

Sanda DespaDepartment of Pharmacology, University of California, Davis, CA, USA. sdespa@ucdavis.edu
Donald M Bers

Funding

Program AdministrationP01HL080101 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERS, DONALD M · 2006 to 2015
$23.4M
Phospholemman and Na-Pump Function in Cardiac MyocytesR01HL081562 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERS, DONALD M · 2005 to 2018
$5.3M
IONIC CONTROL OF CARDIAC MUSCLE CONTRACTION: EC COUPLINGR37HL030077 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERS, DONALD M · 2005 to 2014
$3.9M
Mechanisms of cardiac Ca dysregulation and arrhythmias in ankyrin B deficiencyR01HL109501 · NHLBI · UNIVERSITY OF KENTUCKY · PI DESPA, SANDA · 2011 to 2015
$1.9M
NHLBI NIH HHS HL-109501NHLBI NIH HHS HL-81526NHLBI NIH HHS P01 HL080101NHLBI NIH HHS R01 HL081562NHLBI NIH HHS R01 HL109501NHLBI NIH HHS R37 HL030077
6 · The paper itself

Abstract

In the heart, intracellular Na(+) concentration ([Na(+)]i) is a key modulator of Ca(2+) cycling, contractility and cardiac myocyte metabolism. Several Na(+) transporters are electrogenic, thus they both contribute to shaping the cardiac action potential and at the same time are affected by it. [Na(+)]i is controlled by the balance between Na(+) influx through various pathways, including the Na(+)/Ca(2+) exchanger and Na(+) channels, and Na(+) extrusion via the Na(+)/K(+)-ATPase. [Na(+)]i is elevated in HF due to a combination of increased entry through Na(+) channels and/or Na(+)/H(+) exchanger and reduced activity of the Na(+)/K(+)-ATPase. Here we review the major Na(+) transport pathways in cardiac myocytes and how they participate in regulating [Na(+)]i in normal and failing hearts. This article is part of a Special Issue entitled "Na(+) Regulation in Cardiac Myocytes."

Indexed as

Action PotentialsAnimalsBiological TransportHeart FailureHumansMyocardial ContractionMyocytes, CardiacSodiumSodium-Calcium ExchangerSodium-Potassium-Exchanging ATPaseVoltage-Gated Sodium ChannelsSodiumSodium-Calcium ExchangerSodium-Potassium-Exchanging ATPaseVoltage-Gated Sodium Channelsaction potentialAPCa(2+)/calmodulin dependent kinase II[Ca(2+)](i)[Ca(2+)](m)CaMKIIconcentration of free Ca(2+) in the cytosolconcentration of free Ca(2+) in the mitochondrial matrixDADdelayed afterdepolarizationfamily of proteins that are specific Na/K-ATPase regulatorsFXYDHeart failureintracellular Na(+) concentrationIntracellular Na(+) concentrationMyocyteNa(+)/Ca(2+) exchangerNa(+)/HCO(3)(−) cotransporterNa(+)/H(+) exchanger[Na(+)](i)Na(+)/K(+)-ATPaseNBCNCXNHENKAphospholemmanPLMryanodine receptorRyRsarcoplasmic reticulumSRTMtransmembrane domain

Identifiers

PMID23608603
PMCPMC3720717

What OpenQuestion holds

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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.