Evidence map›Paper›PMID 29024896›Full record

ArticleRedox biology2018

Identification of a soluble guanylate cyclase in RBCs: preserved activity in patients with coronary artery disease.

Miriam M Cortese-Krott, Evanthia Mergia, Christian M Kramer, Wiebke Lückstädt, Jiangning Yang, Georg Wolff, Christina Panknin, Thilo Bracht, Barbara Sitek, John Pernow and 4 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

30 citing papers in PubMed, 69 citations in OpenAlex.

  1. Trial
  2. Review
  3. Erythrocytes as a Source of Exerkines.International journal of molecular sciences · 2025
    Review
  4. Review
  5. THRA1/PGC-1α/SIRT3 pathway regulates oxidative stress and is implicated in hypertension of maternal hypothyroid rat offspring.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Loss of PKGIβ/IRAG1 Signaling Causes Anemia-Associated Splenomegaly.International journal of molecular sciences · 2021
    Article
  11. Article
  12. Article
  13. Soluble Guanylate Cyclase Stimulators and Activators.Handbook of experimental pharmacology · 2021
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. 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

14 authors at 6 institutions in 3 countries.

Miriam M Cortese-KrottCardiovascular Research Laboratory, Division of Cardiology, Pneumology and Vascular Medicine, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225 Düsseldorf, Germany; CARID, Cardiovascular Research Institute Düsseldorf, Medical Faculty, Heinrich Heine University, Moorensstraße 5, 40225 Düsseldorf, Germany. Electronic address: miriam.cortese@uni-duesseldorf.de.
Evanthia MergiaInstitute for Pharmacology and Toxicology, Ruhr-University Bochum, Universitätsstraße 150, 44801 Bochum, Germany.
Christian M KramerCardiovascular Research Laboratory, Division of Cardiology, Pneumology and Vascular Medicine, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225 Düsseldorf, Germany; CARID, Cardiovascular Research Institute Düsseldorf, Medical Faculty, Heinrich Heine University, Moorensstraße 5, 40225 Düsseldorf, Germany.
Wiebke LückstädtCardiovascular Research Laboratory, Division of Cardiology, Pneumology and Vascular Medicine, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225 Düsseldorf, Germany; CARID, Cardiovascular Research Institute Düsseldorf, Medical Faculty, Heinrich Heine University, Moorensstraße 5, 40225 Düsseldorf, Germany.
Jiangning YangDepartment of Medicine, Karolinska Institutet, Karolinska University Hospital, Karolinska Universitetssjukhuset, Solna, 171 76 Stockholm, Sweden.
Georg WolffCardiovascular Research Laboratory, Division of Cardiology, Pneumology and Vascular Medicine, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225 Düsseldorf, Germany; CARID, Cardiovascular Research Institute Düsseldorf, Medical Faculty, Heinrich Heine University, Moorensstraße 5, 40225 Düsseldorf, Germany.
Christina PankninCardiovascular Research Laboratory, Division of Cardiology, Pneumology and Vascular Medicine, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225 Düsseldorf, Germany; CARID, Cardiovascular Research Institute Düsseldorf, Medical Faculty, Heinrich Heine University, Moorensstraße 5, 40225 Düsseldorf, Germany.
Thilo BrachtMedizinisches Proteom-Center, Ruhr- University Bochum, Universitätsstraße 150, 44801 Bochum, Germany.
Barbara SitekMedizinisches Proteom-Center, Ruhr- University Bochum, Universitätsstraße 150, 44801 Bochum, Germany.
John PernowDepartment of Medicine, Karolinska Institutet, Karolinska University Hospital, Karolinska Universitetssjukhuset, Solna, 171 76 Stockholm, Sweden.
Johannes-Peter StaschBayer Pharma AG, Aprather Weg 18a, 42096 Wuppertal, Germany; Institute of Pharmacy, University Halle-Wittenberg, Wolfgang-Langenbeck-Strasse 4, 06120 Halle (Saale), Germany.
Martin FeelischClinical & Experimental Sciences, Faculty of Medicine, University of Southampton, Tremona Road, SO166YD Southampton, United Kingdom.
Doris KoeslingInstitute for Pharmacology and Toxicology, Ruhr-University Bochum, Universitätsstraße 150, 44801 Bochum, Germany.
Malte KelmCardiovascular Research Laboratory, Division of Cardiology, Pneumology and Vascular Medicine, Medical Faculty, Heinrich Heine University, Moorenstraße 5, 40225 Düsseldorf, Germany; CARID, Cardiovascular Research Institute Düsseldorf, Medical Faculty, Heinrich Heine University, Moorensstraße 5, 40225 Düsseldorf, Germany.
Heinrich Heine University Düsseldorf · DERuhr University Bochum · DEKarolinska Institutet · SEKarolinska University Hospital · SEMartin Luther University Halle-Wittenberg · DEUniversity of Southampton · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial dysfunction is associated with decreased NO bioavailability and impaired activation of the NO receptor soluble guanylate cyclase (sGC) in the vasculature and in platelets. Red blood cells (RBCs) are known to produce NO under hypoxic and normoxic conditions; however evidence of expression and/or activity of sGC and downstream signaling pathway including phopshodiesterase (PDE)-5 and protein kinase G (PKG) in RBCs is still controversial. In the present study, we aimed to investigate whether RBCs carry a functional sGC signaling pathway and to address whether this pathway is compromised in coronary artery disease (CAD). Using two independent chromatographic procedures, we here demonstrate that human and murine RBCs carry a catalytically active α

Indexed as

AdultAgedAnimalsCoronary Artery DiseaseCyclic GMPCyclic GMP-Dependent Protein KinasesErythrocytesHumansMiceMiddle AgedNitric OxideSignal TransductionSoluble Guanylyl CyclaseCyclic GMPCyclic GMP-Dependent Protein KinasesNitric OxideSoluble Guanylyl CyclasecGMPNitric oxideNon -canonical functions of RBCsProtein kinase GSignaling

Identifiers

PMID29024896
PMCPMC5975213
OpenAlexW2753549977

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.