Evidence map›Paper›PMID 17510185›Full record

ArticleThe Journal of physiology2007

Protein kinase A is activated by the n-3 polyunsaturated fatty acid eicosapentaenoic acid in rat ventricular muscle.

Norbert Szentandrássy, M R Pérez-Bido, E Alonzo, N Negretti, Stephen C O'Neill

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 31 citations in OpenAlex.

  1. PUFAs regulate SREBP1c through phosphorylation of Insig2.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  2. Phosphorylation of Insig-2 mediates inhibition of fatty acid synthesis by polyunsaturated fatty acids.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
  4. Article
  5. Unknown biological effects of L-glucose, ALA, and PUFA.The journal of physiological sciences : JPS · 2017
    Review
  6. Cardioprotective effects of omega 3 fatty acids: origin of the variability.Journal of muscle research and cell motility · 2017
    Review
  7. Review
  8. Neuron membrane trafficking and protein kinases involved in autism and ADHD.International journal of molecular sciences · 2015
    Review
  9. Article
  10. Article
  11. Article
  12. What we know and do not know about sex and cardiac disease.Journal of biomedicine & biotechnology · 2010
    Review
  13. 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

5 authors at 3 institutions in 2 countries.

Norbert SzentandrássyDepartment of Medicine, University of Manchester, Core Technology Facility, Grafton Street, Manchester M13 9PT, UK.
M R Pérez-Bido
E Alonzo
N Negretti
Stephen C O'Neill
Central University of Venezuela · VEUniversity of Manchester · GBHospital Clínico Universitario de Caracas · VE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During cardiac ischaemia antiarrhythmic n-3 polyunsaturated fatty acids (PUFAs) are released following activation of phospholipase A2, if they are in the diet prior to ischaemia. Here we show a positive lusitropic effect of one such PUFA, eicosapentaenoic acid (EPA) in the antiarrhythmic concentration range in Langendorff hearts and isolated rat ventricular myocytes due to activation of protein kinase A (PKA). Several different approaches indicated activation of PKA by EPA (5-10 micromol l(-1)): the time constant of decay of the systolic Ca2+ transient decreased to 65.3 +/- 5.0% of control, Western blot analysis showed a fourfold increase in phospholamban phosphorylation, and PKA activity increased by 21.0 +/- 7.3%. In addition myofilament Ca2+ sensitivity was reduced in EPA; this too may have resulted from PKA activation. We also found that EPA inhibited L-type Ca2+ current by 38.7 +/- 3.9% but this increased to 63.3 +/- 3.4% in 10 micromol l(-1) H89 (to inhibit PKA), providing further evidence of activation of PKA by EPA. PKA inhibition also prevented the lusitropic effect of EPA on the systolic Ca2+ transient and contraction. Our measurements show, however, PKA activation in EPA cannot be explained by increased cAMP levels and alternative mechanisms for PKA activation are discussed. The combined lusitropic effect and inhibition of contraction by EPA may, respectively, combat diastolic dysfunction in ischaemic cardiac muscle and promote cell survival by preserving ATP. This is a further level of protection for the heart in addition to the well-documented antiarrhythmic qualities of these fatty acids.

Indexed as

Calcium SignalingMyocardial ContractionActin CytoskeletonAction PotentialsAnimalsAnti-Arrhythmia AgentsCalcium-Binding ProteinsCalcium Channels, L-TypeCyclic AMP-Dependent Protein KinasesDepression, ChemicalDose-Response Relationship, DrugEicosapentaenoic AcidEnzyme ActivationHeartHeart VentriclesIn Vitro TechniquesAnti-Arrhythmia AgentsCalcium-Binding ProteinsCalcium Channels, L-TypeCyclic AMP-Dependent Protein KinasesEicosapentaenoic AcidIsoquinolinesN-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamidePhospholambanProtein Kinase InhibitorsSulfonamides

Identifiers

PMID17510185
PMCPMC1976381
OpenAlexW2160562415

What OpenQuestion holds

Textmetadata
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.