Evidence map›Paper›PMID 29294328›Full record

ArticleJournal of molecular and cellular cardiology2018

Improvement of cardiomyocyte function by a novel pyrimidine-based CaMKII-inhibitor.

Stefan Neef, Alexander Steffens, Patricia Pellicena, Julian Mustroph, Simon Lebek, Katharina R Ort, Howard Schulman, Lars S Maier

Open access · hybridAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Enhanced Late IInternational journal of molecular sciences · 2024
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. CaMKII as a Therapeutic Target in Cardiovascular Disease.Annual review of pharmacology and toxicology · 2023
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Chronic CaThe Journal of pharmacology and experimental therapeutics · 2021
    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

8 authors at 2 institutions in 1 country.

Stefan NeefDept. of Internal Medicine II, University Medical Center Regensburg, Regensburg, Germany.
Alexander SteffensDept. of Cardiology and Pneumology, University Medical Center Göttingen, Göttingen, Germany.
Patricia PellicenaAllosteros Therapeutics, Inc., Sunnyvale, CA, USA.
Julian MustrophDept. of Internal Medicine II, University Medical Center Regensburg, Regensburg, Germany.
Simon LebekDept. of Internal Medicine II, University Medical Center Regensburg, Regensburg, Germany.
Katharina R OrtDept. of Thoracic, Cardiac and Vascular Surgery, University Medical Center Göttingen, Göttingen, Germany.
Howard SchulmanAllosteros Therapeutics, Inc., Sunnyvale, CA, USA.
Lars S MaierDept. of Internal Medicine II, University Medical Center Regensburg, Regensburg, Germany. Electronic address: lars.maier@ukr.de.
University Hospital Regensburg · DEUniversitätsmedizin Göttingen · DE

Funding

Optimizing active site inhibitor of CaMKII: A Novel Target in Atrial FibrillationR43HL131089 · NHLBI · ALLOSTEROS THERAPEUTICS, INC. · PI SCHULMAN, HOWARD · 2016 to 2016
$249k
NHLBI NIH HHS R43 HL131089
6 · The paper itself

Abstract

objectivePathologically increased activity of Ca METHODS AND

resultsOur findings demonstrate that AS105 is a high-affinity ATP-competitive CaMKII-inhibitor that by its mode of action is also effective against autophosphorylated CaMKII (in contrast to the commonly used allosteric CaMKII-inhibitor KN-93). In isolated atrial cardiomyocytes from human donors and ventricular myocytes from CaMKIIδ

conclusionAS105 is a novel, highly potent ATP-competitive CaMKII inhibitor. In vitro, it effectively reduced SR Ca

Indexed as

AnimalsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channels, L-TypeExcitation Contraction CouplingHumansMice, Inbred C57BLMyocytes, CardiacProtein Kinase InhibitorsPyrimidinesSarcoplasmic ReticulumCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channels, L-TypeProtein Kinase InhibitorspyrimidinePyrimidinesCa(2+) handlingCaMKIIHeart failure

Identifiers

PMID29294328
PMCPMC5820112
OpenAlexW2781089679

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.