Evidence map›Paper›PMID 29905892›Full record

ReviewBasic research in cardiology2018

Physiological and unappreciated roles of CaMKII in the heart.

Jan Beckendorf, Maarten M G van den Hoogenhof, Johannes Backs

Open access · hybridAbstract readReview
In one paragraph

Review in Basic research in cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
11.3field-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

93 citing papers in PubMed, 166 citations in OpenAlex.

  1. Review
  2. Review
  3. Precision modification of heart failure signaling by CRISPR-Cas9 base editing.Journal of molecular and cellular cardiology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. CaPhysiological reports · 2026
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Cytoplasmic CaMKIIδ-B prevents myocardial recovery in heart failure.bioRxiv : the preprint server for biology · 2025
    Article
  18. Increased MyocardialInternational journal of molecular sciences · 2025
    Article
  19. Article
  20. Mitochondrial dysfunction as a central hub linking NaFrontiers in cardiovascular medicine · 2025
    Review

33 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

3 authors at 2 institutions in 1 country.

Jan BeckendorfDepartment for Molecular Cardiology and Epigenetics, University Hospital Heidelberg, Im Neuenheimer Feld 669, 69120, Heidelberg, Germany.
Maarten M G van den HoogenhofDepartment for Molecular Cardiology and Epigenetics, University Hospital Heidelberg, Im Neuenheimer Feld 669, 69120, Heidelberg, Germany.
Johannes BacksDepartment for Molecular Cardiology and Epigenetics, University Hospital Heidelberg, Im Neuenheimer Feld 669, 69120, Heidelberg, Germany. Johannes.backs@med.uni-heidelberg.de.
German Centre for Cardiovascular Research · DEUniversity Hospital Heidelberg · DE

Funding

Deutsche Forschungsgemeinschaft SFB 1118
6 · The paper itself

Abstract

In the cardiomyocyte, CaMKII has been identified as a nodal influencer of excitation-contraction and also excitation-transcription coupling. Its activity can be regulated in response to changes in intracellular calcium content as well as after several post-translational modifications. Some of the effects mediated by CaMKII may be considered adaptive, while effects of sustained CaMKII activity may turn into the opposite and are detrimental to cardiac integrity and function. As such, CaMKII has long been noted as a promising target for pharmacological inhibition, but the ubiquitous nature of CaMKII has made it difficult to target CaMKII specifically where it is detrimental. In this review, we provide a brief overview of the physiological and pathophysiological properties of CaMKII signaling, but we focus on the physiological and adaptive functions of CaMKII. Furthermore, special consideration is given to the emerging role of CaMKII as a mediator of inflammatory processes in the heart.

Indexed as

AnimalsApoptosisCalcium-Calmodulin-Dependent Protein Kinase Type 2Chagas CardiomyopathyEnzyme ActivationGene Expression Regulation, EnzymologicHumansInflammation MediatorsMyocarditisMyocardiumNecrosisProtein ConformationSignal TransductionStructure-Activity RelationshipCalcium-Calmodulin-Dependent Protein Kinase Type 2Inflammation MediatorsApoptosisCalciumCalmodulinCaMKIICardiomyocyteInflammation

Identifiers

PMID29905892
PMCPMC6003982
OpenAlexW2807811843

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.