Evidence map›Paper›PMID 26379551›Full record

ReviewFrontiers in pharmacology2015

Regulation of CaMKII signaling in cardiovascular disease.

Mariya Y Mollova, Hugo A Katus, Johannes Backs

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Review
  3. Calmodulin: a highly conserved and ubiquitous CaProceedings of the Japan Academy. Series B, Physical and biological sciences · 2024
    Review
  4. Article
  5. Reduced O-GlcNAcylation diminishes cardiomyocyte CaJournal of molecular and cellular cardiology · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Ligand-activated RXFP1 gene therapy ameliorates pressure overload-induced cardiac dysfunction.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
  11. Chronic CaThe Journal of pharmacology and experimental therapeutics · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Oxidative Stress in Radiation-Induced Cardiotoxicity.Oxidative medicine and cellular longevity · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. Article
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.

Mariya Y MollovaResearch Unit Cardiac Epigenetics, Department of Cardiology, Angiology and Pneumology, University of Heidelberg , Heidelberg, Germany ; Department of Cardiology, Angiology and Pneumology, University of Heidelberg , Heidelberg, Germany ; Partner Site Heidelberg/Mannheim, German Center for Cardiovascular Research , Heidelberg, Germany.
Hugo A KatusDepartment of Cardiology, Angiology and Pneumology, University of Heidelberg , Heidelberg, Germany ; Partner Site Heidelberg/Mannheim, German Center for Cardiovascular Research , Heidelberg, Germany.
Johannes BacksResearch Unit Cardiac Epigenetics, Department of Cardiology, Angiology and Pneumology, University of Heidelberg , Heidelberg, Germany ; Partner Site Heidelberg/Mannheim, German Center for Cardiovascular Research , Heidelberg, Germany.
Heidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure (HF) is a major cause of death in the developed countries (Murray and Lopez, 1996; Koitabashi and Kass, 2012). Adverse cardiac remodeling that precedes heart muscle dysfunction is characterized by a myriad of molecular changes affecting the cardiomyocyte. Among these, alterations in protein kinase pathways play often an important mediator role since they link upstream pathologic stress signaling with downstream regulatory programs and thus affect both the structural and functional integrity of the heart muscle. In the context of cardiac disease, a profound understanding for the overriding mechanisms that regulate protein kinase activity (protein-protein interactions, post-translational modifications, or targeting via anchoring proteins) is crucial for the development of specific and effective pharmacological treatment strategies targeting the failing myocardium. In this review, we focus on several mechanisms of upstream regulation of Ca(2+)-calmodulin-dependent protein kinase II that play a relevant pathophysiological role in the development and progression of cardiovascular disease; precise targeting of these mechanisms might therefore represent novel and promising tools for prevention and treatment of HF.

Indexed as

CaMKIIenzymatic activityheart failurepost-translational modificationssub-cellular localization

Identifiers

PMID26379551
PMCPMC4548452
OpenAlexW1918725443

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.