Evidence map›Paper›PMID 23789646›Full record

ReviewExpert opinion on therapeutic targets2013

The promise of CaMKII inhibition for heart disease: preventing heart failure and arrhythmias.

B Daan Westenbrink, Andrew G Edwards, Andrew D McCulloch, Joan Heller Brown

Open access · greenAbstract readReview
In one paragraph

Review in Expert opinion on therapeutic targets, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Red light-green light: T-cell trafficking in cardiac and vascular inflammation.American journal of physiology. Cell physiology · 2023
    Review
  3. Article
  4. Article
  5. Emerging therapeutic targets for cardiac hypertrophy.Expert opinion on therapeutic targets · 2022
    Review
  6. Article
  7. ATPase Inhibitory Factor-1 Disrupts Mitochondrial CaInternational journal of molecular sciences · 2021
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. 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

4 authors at 3 institutions in 2 countries.

B Daan WestenbrinkUniversity of California, Department of Pharmacology, San Diego, La Jolla, CA, USA.
Andrew G Edwards
Andrew D McCulloch
Joan Heller Brown
La Jolla Bioengineering Institute · USUniversity of California, San Diego · USUniversity of Groningen · NL

Funding

Program AdministrationP01HL080101 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERS, DONALD M · 2006 to 2015
$23.4M
Multi-scale Systems Model of Murine Heart FailureR01HL105242 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BERS, DONALD M, MCCULLOCH, ANDREW D. · 2012 to 2016
$3.5M
NHLBI NIH HHS HL080101NHLBI NIH HHS HL105242NHLBI NIH HHS P01 HL080101NHLBI NIH HHS R01 HL105242
6 · The paper itself

Abstract

introductionCalcium-calmodulin-dependent protein kinase II (CaMKII) has emerged as a central mediator of cardiac stress responses which may serve several critical roles in the regulation of cardiac rhythm, cardiac contractility and growth. Sustained and excessive activation of CaMKII during cardiac disease has, however, been linked to arrhythmias, and maladaptive cardiac remodeling, eventually leading to heart failure (HF) and sudden cardiac death. AREAS COVERED: In the current review, the authors describe the unique structural and biochemical properties of CaMKII and focus on its physiological effects in cardiomyocytes. Furthermore, they provide evidence for a role of CaMKII in cardiac pathologies, including arrhythmogenesis, myocardial ischemia and HF development. The authors conclude by discussing the potential for CaMKII as a target for inhibition in heart disease. EXPERT OPINION: CaMKII provides a promising nodal point for intervention that may allow simultaneous prevention of HF progression and development of arrhythmias. For future studies and drug development there is a strong rationale for the development of more specific CaMKII inhibitors. In addition, an improved understanding of the differential roles of CaMKII subtypes is required.

Indexed as

AnimalsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Heart DiseasesHumansProtein Kinase InhibitorsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Protein Kinase Inhibitors

Identifiers

PMID23789646
PMCPMC5551677
OpenAlexW2114937126

What OpenQuestion holds

Textmetadata
LicenceTDM
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.