Evidence map›Paper›PMID 23808942›Full record

ArticleBritish journal of pharmacology2013

SERCA2 activity is involved in the CNP-mediated functional responses in failing rat myocardium.

L R Moltzau, J M Aronsen, S Meier, C H T Nguyen, K Hougen, Ø Ørstavik, I Sjaastad, G Christensen, T Skomedal, J-B Osnes and 2 more

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In one paragraph

Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  3. Cardiac Roles of Serotonin (5-HT) and 5-HT-Receptors in Health and Disease.International journal of molecular sciences · 2023
    Review
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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

12 authors at 3 institutions in 1 country.

L R MoltzauDepartment of Pharmacology, Faculty of Medicine, University of Oslo and Oslo University Hospital, Oslo, Norway; KG Jebsen Cardiac Research Centre and Center for Heart Failure Research, Faculty of Medicine, University of Oslo, Oslo, Norway.
J M Aronsen
S Meier
C H T Nguyen
K Hougen
Ø Ørstavik
I Sjaastad
G Christensen
T Skomedal
J-B Osnes
F O Levy
E Qvigstad
University of Oslo · NOOslo University Hospital · NOInstitutt for Eksperimentell Medisinsk Forskning · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposesMyocardial C-type natriuretic peptide (CNP) levels are increased in heart failure. CNP can induce negative inotropic (NIR) and positive lusitropic responses (LR) in normal hearts, but its effects in failing hearts are not known. We studied the mechanism of CNP-induced NIR and LR in failing hearts and determined whether sarcoplasmatic reticulum Ca(2+) ATPase2 (SERCA2) activity is essential for these responses. EXPERIMENTAL APPROACH: Contractility, cGMP levels, Ca(2+) transient amplitudes and protein phosphorylation were measured in left ventricular muscle strips or ventricular cardiomyocytes from failing hearts of Wistar rats 6 weeks after myocardial infarction. KEY

resultsCNP increased cGMP levels, evoked a NIR and LR in muscle strips, and caused phospholamban (PLB) Ser(16) and troponin I (TnI) Ser(23/24) phosphorylation in cardiomyocytes. Both the NIR and LR induced by CNP were reduced in the presence of a PKG blocker/cGMP analogue (Rp-8-Br-Pet-cGMPS) and the SERCA inhibitor thapsigargin. CNP increased the amplitude of the Ca(2+) transient and increased SERCA2 activity in cardiomyocytes. The CNP-elicited NIR and LR were not affected by the L-type Ca(2+) channel activator BAY-K8644, but were abolished in the presence of isoprenaline (induces maximal activation of cAMP pathway). This suggests that phosphorylation of PLB and TnI by CNP causes both a NIR and LR. The NIR to CNP in mouse heart was abolished 8 weeks after cardiomyocyte-specific inactivation of the SERCA2 gene. CONCLUSIONS AND IMPLICATIONS: We conclude that CNP-induced PLB and TnI phosphorylation by PKG in concert mediate both a predictable LR as well as the less expected NIR in failing hearts.

Indexed as

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl esterAnimalsCalcium-Binding ProteinsCyclic GMPCyclic GMP-Dependent Protein KinasesHeart FailureIsoproterenolMaleMiceMice, KnockoutMyocardial InfarctionMyocardiumMyocytes, CardiacNatriuretic Peptide, C-TypePhospholambanPhosphorylation3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester8-bromo-beta-phenyl-1,N(2)-ethenoguanosine 3',5'-cyclic monophosphorothioateAtp2a2 protein, mouseAtp2a2 protein, ratCalcium-Binding ProteinsCyclic GMPCyclic GMP-Dependent Protein KinasesIsoproterenolNatriuretic Peptide, C-TypePhospholambanSarcoplasmic Reticulum Calcium-Transporting ATPasesThapsigarginThionucleotidesTroponin IC-type natriuretic peptideheart failurelusitropic responsenegative inotropic responsesarcoplasmatic reticulum Ca2+ ATPasetroponin I

Identifiers

PMID23808942
PMCPMC3834760
OpenAlexW1537905458

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.