Evidence map›Paper›PMID 16955136›Full record

ArticleThe Journal of clinical investigation2006

Deconstructing endothelial dysfunction: soluble guanylyl cyclase oxidation and the NO resistance syndrome.

Mark T Gladwin

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.4field-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

34 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Soluble Guanylate Cyclase Stimulators and Activators.Handbook of experimental pharmacology · 2021
    Article
  9. Observational
  10. Review
  11. Pathophysiology of Sickle Cell Disease.Annual review of pathology · 2019
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Soluble guanylate cyclase as an alternative target for bronchodilator therapy in asthma.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Mark T GladwinVascular Medicine Branch, National Heart, Lung, and Blood Institute, and Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, Maryland 20892, USA. mgladwin@nih.gov
National Heart Lung and Blood Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In this issue of the JCI, Stasch and colleagues suggest that a novel drug, BAY 58-2667, potently activates a pool of oxidized and heme-free soluble guanylyl cyclase (sGC; see the related article beginning on page 2552). The increased vasodilatory potency of BAY 58-2667 the authors found in a number of animal models of endothelial dysfunction and in human blood vessels from patients with diabetes suggests that there exists a subphenotype of endothelial dysfunction characterized by receptor-level NO resistance. Diseases associated with NO resistance would appear to be ideally suited for therapies directed at restoring redox homeostasis, sGC activity, and NO sensitivity.

Indexed as

AnimalsBenzoatesCyclic GMPEndothelium, VascularGuanylate CyclaseHumansNitric OxideOxidation-ReductionReceptors, Cytoplasmic and NuclearSoluble Guanylyl CyclaseVasodilationBAY 58-2667BenzoatesCyclic GMPGuanylate CyclaseNitric OxideReceptors, Cytoplasmic and NuclearSoluble Guanylyl Cyclase

Identifiers

PMID16955136
PMCPMC1555666
OpenAlexW1986547098

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.