Evidence map›Paper›PMID 23108187›Full record

ReviewJournal of molecular and cellular cardiology2013

Store-dependent deactivation: cooling the chain-reaction of myocardial calcium signaling.

Przemysław B Radwański, Andriy E Belevych, Lucia Brunello, Cynthia A Carnes, Sándor Györke

Open access · greenAbstract 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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 12% 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, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Neuronal NaJACC. Basic to translational science · 2016
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Ibandronate and ventricular arrhythmia risk.Journal of cardiovascular electrophysiology · 2014
    Article
  14. Article
  15. Decreased RyR2 refractoriness determines myocardial synchronization of aberrant Ca2+ release in a genetic model of arrhythmia.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  16. 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

5 authors at 1 institution in 1 country.

Przemysław B RadwańskiThe Dorothy M. Davis Heart and Lung Research Institute, Department of Physiology and Cell Biology, The Ohio State University, Columbus, OH, USA.
Andriy E Belevych
Lucia Brunello
Cynthia A Carnes
Sándor Györke
The Ohio State University · US

Funding

CONTROLLED AND UNCONTROLLABLE CALCIUM RELEASE IN HEARTR01HL063043 · NHLBI · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI Sandor Gyorke · 1999 to 2026
$8.6M
Ryanodine Receptor Channels in Heart FailureR01HL074045 · NHLBI · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI GYORKE, SANDOR · 2003 to 2024
$8.2M
Heart Failure and Atrial FibrillationR01HL089836 · NHLBI · OHIO STATE UNIVERSITY · PI CARNES, CYNTHIA A · 2008 to 2012
$2.1M
NHLBI NIH HHS HL063043NHLBI NIH HHS HL074045NHLBI NIH HHS HL089836NHLBI NIH HHS R01 HL063043NHLBI NIH HHS R01 HL074045NHLBI NIH HHS R01 HL089836
6 · The paper itself

Abstract

In heart cells, Ca(2+) released from the internal storage unit, the sarcoplasmic reticulum (SR) through ryanodine receptor (RyR2) channels is the predominant determinant of cardiac contractility. Evidence obtained in recent years suggests that SR Ca(2+) release is tightly regulated not only by cytosolic Ca(2+) but also by intra-store Ca(2+) concentration. Specifically, Ca(2+)-induced Ca(2+) release (CICR) that relies on auto-catalytic action of Ca(2+) at the cytosolic side of RyR2s is precisely balanced and counteracted by RyR2 deactivation dependent on a reciprocal decrease of Ca(2+) at the luminal side of RyR2s. Dysregulation of this inherently unstable Ca(2+) signaling is considered to be an underlying cause of triggered arrhythmias, and is associated with genetic and acquired forms of sudden cardiac death. In this article, we present an overview of recent advances in our understanding of the regulatory role luminal Ca(2+) plays in Ca(2+) handling, with a particular emphasis on the role of Ca(2+)release refractoriness in aberrant Ca(2+) release.

Indexed as

Calcium SignalingArrhythmias, CardiacCalciumDeath, Sudden, CardiacHumansMyocardiumMyocytes, CardiacRyanodine Receptor Calcium Release ChannelSarcoplasmic ReticulumCalciumRyanodine Receptor Calcium Release Channel

Identifiers

PMID23108187
PMCPMC4068615
OpenAlexW2041711276

What OpenQuestion holds

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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.