Evidence map›Paper›PMID 22932727›Full record

ReviewHeart failure reviews2013

The ryanodine receptor leak: how a tattered receptor plunges the failing heart into crisis.

Thomas H Fischer, Lars S Maier, Samuel Sossalla

Abstract readReview
In one paragraph

Review in Heart failure reviews, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Trial
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  3. Article
  4. Review
  5. Sex-dependent remodeling of right ventricular function in a rat model of pulmonary arterial hypertension.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  6. Review
  7. Article
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  11. Article
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  16. Article
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  19. TRP Channels Mediated Pathological CaFrontiers in cardiovascular medicine · 2019
    Review
  20. 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.

Thomas H FischerDepartment of Cardiology and Pneumology, Heart Center, Georg-August-University Göttingen, Robert-Koch-Str. 40, 37075 Göttingen, Germany.
Lars S Maier
Samuel Sossalla

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been persuasively shown in the last two decades that the development of heart failure is closely linked to distinct alterations in Ca(2+) cycling. A crucial point in this respect is an increased spontaneous release of Ca(2+) out of the sarcoplasmic reticulum during diastole via ryanodine receptors type 2 (RyR2). The consequence is a compromised sarcoplasmic reticulum Ca(2+) storage capacity, which impairs systolic contractility and possibly diastolic cardiac function due to Ca(2+) overload. Additionally, leaky RyR2 are more and more regarded to potently induce proarrhythmic triggers. Elimination of spontaneously released Ca(2+) via RyR2 in diastole can cause a transient sarcolemmal inward current and hence delayed after depolarisations as substrate for cardiac arrhythmias. In this article, the pathological role and consequences of the SR Ca(2+)-leak and its regulation are reviewed with a main focus on protein kinase A and Ca(2+)-calmodulin-dependent kinase II. We summarise clinical consequences of "leaky RyR2" as well as possible therapeutic strategies in order to correct RyR2 dysfunction and discuss the significance of the available data.

Indexed as

CalciumCyclic AMP-Dependent Protein KinasesDiastoleHeart FailureHumansMyocytes, CardiacRyanodine Receptor Calcium Release ChannelSarcoplasmic ReticulumCalciumCyclic AMP-Dependent Protein KinasesRyanodine Receptor Calcium Release Channel

Identifiers

PMID22932727
PMCPMC3677980

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Registered trials

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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.