Evidence map›Paper›PMID 29467337›Full record

ArticleJCI insight2018

Nitric oxide-sensitive guanylyl cyclase stimulation improves experimental heart failure with preserved ejection fraction.

Nicola Wilck, Lajos Markó, András Balogh, Kristin Kräker, Florian Herse, Hendrik Bartolomaeus, István A Szijártó, Maik Gollasch, Nadine Reichhart, Olaf Strauss and 11 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.5field-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

28 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Soluble guanylate cyclase stimulators and activators as potential antihypertensive drugs.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Cyclic GMP and PKG Signaling in Heart Failure.Frontiers in pharmacology · 2022
    Review
  15. Article
  16. Review
  17. Article
  18. Soluble Guanylate Cyclase Stimulators and Activators.Handbook of experimental pharmacology · 2021
    Article
  19. 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

21 authors at 3 institutions in 1 country.

Nicola WilckExperimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine and the Charité Medical Faculty, Berlin, Germany.
Lajos MarkóExperimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine and the Charité Medical Faculty, Berlin, Germany.
András BaloghExperimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine and the Charité Medical Faculty, Berlin, Germany.
Kristin KräkerExperimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine and the Charité Medical Faculty, Berlin, Germany.
Florian HerseExperimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine and the Charité Medical Faculty, Berlin, Germany.
Hendrik BartolomaeusExperimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine and the Charité Medical Faculty, Berlin, Germany.
István A SzijártóExperimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine and the Charité Medical Faculty, Berlin, Germany.
Maik GollaschExperimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine and the Charité Medical Faculty, Berlin, Germany.
Nadine ReichhartCharité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, and BIH, Berlin, Germany.
Olaf StraussCharité - Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin, and BIH, Berlin, Germany.
Arnd HeuserMax-Delbrück Center for Molecular Medicine, Berlin, Germany.
Damian BrockschniederBayer AG, Drug Discovery, Wuppertal & Berlin, Germany.
Axel KretschmerBayer AG, Drug Discovery, Wuppertal & Berlin, Germany.
Ralf LescheBayer AG, Drug Discovery, Wuppertal & Berlin, Germany.
Florian SohlerBayer AG, Drug Discovery, Wuppertal & Berlin, Germany.
Johannes-Peter StaschBayer AG, Drug Discovery, Wuppertal & Berlin, Germany.
Peter SandnerBayer AG, Drug Discovery, Wuppertal & Berlin, Germany.
Friedrich C LuftExperimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine and the Charité Medical Faculty, Berlin, Germany.
Dominik N MüllerExperimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine and the Charité Medical Faculty, Berlin, Germany.
Ralf DechendExperimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine and the Charité Medical Faculty, Berlin, Germany.
Nadine HaaseExperimental and Clinical Research Center, Max-Delbrück Center for Molecular Medicine and the Charité Medical Faculty, Berlin, Germany.
Max Delbrück Center · DEBayer (Germany) · DEHumboldt-Universität zu Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure with preserved ejection fraction (HFpEF) can arise from cardiac and vascular remodeling processes following long-lasting hypertension. Efficacy of common HF therapeutics is unsatisfactory in HFpEF. Evidence suggests that stimulators of the nitric oxide-sensitive soluble guanylyl cyclase (NOsGC) could be of use here. We aimed to characterize the complex cardiovascular effects of NOsGC stimulation using NO-independent stimulator BAY 41-8543 in a double-transgenic rat (dTGR) model of HFpEF. We show a drastically improved survival rate of treated dTGR. We observed less cardiac fibrosis, macrophage infiltration, and gap junction remodeling in treated dTGR. Microarray analysis revealed that treatment of dTGR corrected the dysregulateion of cardiac genes associated with fibrosis, inflammation, apoptosis, oxidative stress, and ion channel function toward an expression profile similar to healthy controls. Treatment reduced systemic blood pressure levels and improved endothelium-dependent vasorelaxation of resistance vessels. Further comprehensive in vivo phenotyping showed an improved diastolic cardiac function, improved hemodynamics, and less susceptibility to ventricular arrhythmias. Short-term BAY 41-8543 application in isolated untreated transgenic hearts with structural remodeling significantly reduced the occurrence of ventricular arrhythmias, suggesting a direct nongenomic role of NOsGC stimulation on excitation. Thus, NOsGC stimulation was highly effective in improving several HFpEF facets in this animal model, underscoring its potential value for patients.

Indexed as

Administration, OralAngiotensinogenAnimalsArrhythmias, CardiacBlood PressureChronic DiseaseDisease Models, AnimalDrug Evaluation, PreclinicalEchocardiographyHeart FailureHeart VentriclesHumansIsolated Heart PreparationMaleMorpholinesPyrimidinesAGT protein, humanAngiotensinogenBAY 41-8543MorpholinesPyrimidinesReninSoluble Guanylyl CyclaseCardiologyHeart failure

Identifiers

PMID29467337
PMCPMC5916255
OpenAlexW2788195108

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.