Evidence map›Paper›PMID 17429038›Full record

SynthesisPhysiological reviews2007

Calcium and arrhythmogenesis.

Henk E D J Ter Keurs, Penelope A Boyden

Open access · greenAbstract readSystematic Review
In one paragraph

Synthesis in Physiological reviews, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed
18.3field-weighted citation impact, top 1% 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

180 citing papers in PubMed, 352 citations in OpenAlex.

  1. Review
  2. Increased CaCells · 2026
    Article
  3. Calcium release channel deficiency syndrome in patients diagnosed with idiopathic ventricular fibrillation and decedents classified as sudden unexplained death in the young.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026
    Article
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  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Targeting p21-activated kinase 1 for development of a novel anti-arrhythmic drug class.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  16. Review
  17. Mitochondrial connexin43 and mitochondrial KPflugers Archiv : European journal of physiology · 2023
    Article
  18. Article
  19. Article
  20. Article

120 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 at 1 institution in 1 country.

Henk E D J Ter KeursDepartment of Medicine, Physiology and Biophysics, University of Calgary, Alberta, Canada.
Penelope A Boyden
University of Calgary · CA

Funding

Ion Channel Function in Arrhythmogenic Cardiac CellsR01HL066140 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BOYDEN, PENELOPE ALTMAN · 2001 to 2010
$3.7M
CALCIUM WAVES AND ARRHYTHMIASR01HL058860 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BOYDEN, PENELOPE ALTMAN · 1998 to 2008
$2.9M
NHLBI NIH HHS HL-58860NHLBI NIH HHS HL-66140NHLBI NIH HHS R01 HL058860NHLBI NIH HHS R01 HL066140
6 · The paper itself

Abstract

Triggered activity in cardiac muscle and intracellular Ca2+ have been linked in the past. However, today not only are there a number of cellular proteins that show clear Ca2+ dependence but also there are a number of arrhythmias whose mechanism appears to be linked to Ca2+-dependent processes. Thus we present a systematic review of the mechanisms of Ca2+ transport (forward excitation-contraction coupling) in the ventricular cell as well as what is known for other cardiac cell types. Second, we review the molecular nature of the proteins that are involved in this process as well as the functional consequences of both normal and abnormal Ca2+ cycling (e.g., Ca2+ waves). Finally, we review what we understand to be the role of Ca2+ cycling in various forms of arrhythmias, that is, those associated with inherited mutations and those that are acquired and resulting from reentrant excitation and/or abnormal impulse generation (e.g., triggered activity). Further solving the nature of these intricate and dynamic interactions promises to be an important area of research for a better recognition and understanding of the nature of Ca2+ and arrhythmias. Our solutions will provide a more complete understanding of the molecular basis for the targeted control of cellular calcium in the treatment and prevention of such.

Indexed as

AnimalsArrhythmias, CardiacBiological Transport, ActiveCalciumCalcium SignalingHumansMyocardial ContractionMyocardiumCalcium

Identifiers

PMID17429038
PMCPMC4332537
OpenAlexW2123374731

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.