Evidence map›Paper›PMID 36715019›Full record

ArticleCirculation research2023

CNP Promotes Antiarrhythmic Effects via Phosphodiesterase 2.

Eleder Cachorro, Mario Günscht, Mario Schubert, Mirna S Sadek, Johanna Siegert, Fabian Dutt, Carla Bauermeister, Susann Quickert, Henrik Berning, Felix Nowakowski and 15 more

Open access · hybridAbstract read
In one paragraph

Article in Circulation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

8 citing papers in PubMed, 20 citations in OpenAlex.

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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

25 authors at 8 institutions in 4 countries.

Eleder CachorroInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).
Mario GünschtInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).ORCID 0000-0003-1686-6442
Mario SchubertInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).
Mirna S SadekInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).
Johanna SiegertInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).
Fabian DuttInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).
Carla BauermeisterInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).ORCID 0000-0003-4775-1891
Susann QuickertInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).
Henrik BerningInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).ORCID 0000-0003-1170-7784
Felix NowakowskiInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).
Simon LämmleInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).
Rebecca FirneburgInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).
Xiaojing LuoInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).
Stephan R KünzelInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).
Erik KlapprothInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).
Peter MirtschinkInstitute of Clinical Chemistry and Laboratory Medicine, Department of Clinical Pathobiochemistry, University Hospital Dresden, Germany (P.M.).
Manuel MayrThe James Black Centre, King's College, University of London, United Kingdom (M.M.).ORCID 0000-0002-0597-829X
Matthias DewenterDepartment of Molecular Cardiology and Epigenetics, Heidelberg University, Germany (M.D.).
Christiane VettelDZHK (German Center for Cardiovascular Research), Partner Site, Heidelberg-Mannheim, Germany (M.D., C.V.).
Jordi HeijmanDepartment of Cardiology, CARIM School for Cardiovascular Diseases, Faculty of Health, Medicine, and Life Sciences, Maastricht University, The Netherlands (J.H.).ORCID 0000-0002-1418-108X
Kristina LorenzInstitut für Pharmakologie und Toxikologie, Julius-Maximilians-Universität Würzburg, Germany (K.L.).
Kaomei GuanInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).ORCID 0000-0002-0753-3083
Ali El-ArmoucheInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).ORCID 0000-0003-2514-9429
Michael WagnerInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).
Susanne KämmererInstitut für Pharmakologie und Toxikologie, Technische Universität Dresden, Germany (E.C., M.G., M.S., M.S.S., J.S., F.D., C.B., S.Q., H.B., F.N., S.L., R.F., X.L., S.R.K., E.K., K.G., A.E.-A., M.W., S.K.).
Norwegian Womens Public Health Association · NODeutsches Herzzentrum der Charité · DEHeidelberg University · DEKing's College London · GBMaastricht University · NLMedigene (Germany) · DETechnische Universität Dresden · DEUniversity of Würzburg · DE

Funding

British Heart Foundation CH/16/3/32406
6 · The paper itself

Abstract

backgroundVentricular arrhythmia and sudden cardiac death are the most common lethal complications after myocardial infarction. Antiarrhythmic pharmacotherapy remains a clinical challenge and novel concepts are highly desired. Here, we focus on the cardioprotective CNP (C-type natriuretic peptide) as a novel antiarrhythmic principle. We hypothesize that antiarrhythmic effects of CNP are mediated by PDE2 (phosphodiesterase 2), which has the unique property to be stimulated by cGMP to primarily hydrolyze cAMP. Thus, CNP might promote beneficial effects of PDE2-mediated negative crosstalk between cAMP and cGMP signaling pathways.

methodsTo determine antiarrhythmic effects of cGMP-mediated PDE2 stimulation by CNP, we analyzed arrhythmic events and intracellular trigger mechanisms in mice in vivo, at organ level and in isolated cardiomyocytes as well as in human-induced pluripotent stem cell-derived cardiomyocytes.

resultsIn ex vivo perfused mouse hearts, CNP abrogated arrhythmia after ischemia/reperfusion injury. Upon high-dose catecholamine injections in mice, PDE2 inhibition prevented the antiarrhythmic effect of CNP. In mouse ventricular cardiomyocytes, CNP blunted the catecholamine-mediated increase in arrhythmogenic events as well as in I

conclusionsCNP shows strong PDE2-dependent antiarrhythmic effects. Consequently, the CNP-PDE2 axis represents a novel and attractive target for future antiarrhythmic strategies.

Indexed as

Myocytes, CardiacPhosphoric Diester HydrolasesAnimalsAnti-Arrhythmia AgentsArrhythmias, CardiacCatecholaminesCyclic GMPHumansMiceNatriuretic Peptide, C-TypeSignal TransductionAnti-Arrhythmia AgentsCatecholaminesCyclic GMPNatriuretic Peptide, C-TypePhosphoric Diester Hydrolasescardiomyocytesinfarctionmicemyocytes, cardiacreperfusionsudden cardiac death

Identifiers

PMID36715019
PMCPMC9930893
OpenAlexW4318477039

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.