Evidence map›Paper›PMID 22768959›Full record

ArticleBiophysical journal2012

Can the sodium-calcium exchanger initiate or suppress calcium sparks in cardiac myocytes?

Daisuke Sato, Sanda Despa, Donald M Bers

Open access · bronzeAbstract readLetter
In one paragraph

Article in Biophysical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Article
  6. Article
  7. Article
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  9. Article
  10. Article
  11. Mitochondrial calcium uptake.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Review
  12. Review
  13. Article
  14. Cardiac electrophysiological dynamics from the cellular level to the organ level.Biomedical engineering and computational biology · 2013
    Review
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 1 institution in 1 country.

Daisuke Sato
Sanda Despa
Donald M Bers
University of California, Davis · US

Funding

Pathophysiological Regulation of Cardiac Myocyte RyR ChannelR01HL092097 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Donald M Bers, Robyn T Rebbeck · 2010 to 2026
$9.3M
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
Modeling of Cardiac Calcium Dynamics; Ryanodine Receptor induced ArrhythmiasR00HL111334 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI SATO, DAISUKE · 2015 to 2017
$738k
Modeling of Cardiac Calcium Dynamics; Ryanodine Receptor induced ArrhythmiasK99HL111334 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI SATO, DAISUKE · 2012 to 2013
$194k
NHLBI NIH HHS HL109501NHLBI NIH HHS K99 HL111334NHLBI NIH HHS R00 HL111334NHLBI NIH HHS R01 HL092097NHLBI NIH HHS R01 HL109501NHLBI NIH HHS R37 HL030077NHLBI NIH HHS R37-HL30077
6 · The paper itself

Abstract

Positive feedback of Calcium (Ca)-induced Ca release is the mechanism of Ca spark formation in cardiac myocytes. To initiate this process, a certain amount of Ca in the cleft space is necessary. When the membrane potential becomes higher during excitation-contraction coupling, Ca can enter through both Ca current (I(CaL)) and sodium-calcium exchanger (NCX) and may activate ryanodine receptors to initiate a Ca spark. On the other hand, at the resting membrane potential (V(m) ~-80 mV), NCX removes Ca from the cell (forward mode). If Ca released from the sarcoplasmic reticulum is quickly removed via forward mode NCX before Ca-induced Ca release starts, the Ca release becomes nonspark Ca leak. This would also be influenced by the cleft/noncleft distribution of NCX, which is unknown. Using a physiologically detailed mathematical model of subcellular Ca cycling, we analyze how NCX strength and distribution alter Ca spark formation. During excitation-contraction coupling, most Ca sparks are induced by I(CaL) with very few due to NCX current. At the resting membrane potential if most NCX is localized to the cleft, spontaneous Ca sparks are significantly reduced.

Indexed as

Calcium SignalingElectric ConductivityModels, BiologicalMyocytes, CardiacRyanodine Receptor Calcium Release ChannelSarcoplasmic ReticulumSodium-Calcium ExchangerRyanodine Receptor Calcium Release ChannelSodium-Calcium Exchanger

Identifiers

PMID22768959
PMCPMC3328690
OpenAlexW2011980257

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.