Evidence map›Paper›PMID 40559470›Full record

ArticlePathophysiology : the official journal of the International Society for Pathophysiology2025

A Slow Hydrogen Sulfide Donor GYY-4137 Partially Improves Vascular Function in Spontaneously Hypertensive Rats Fed a High-Fat Diet.

Basak G Aydemir, Andrea Berenyiova, Martina Cebova, John D Henderson, Andrej Barta, Sona Cacanyiova

Abstract read
In one paragraph

Article in Pathophysiology : the official journal of the International Society for Pathophysiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. 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

6 authors.

Basak G AydemirInstitute of Normal and Pathological Physiology, Centre of Experimental Medicine, Slovak Academy of Sciences, 841 04 Bratislava, Slovakia.
Andrea BerenyiovaInstitute of Normal and Pathological Physiology, Centre of Experimental Medicine, Slovak Academy of Sciences, 841 04 Bratislava, Slovakia.ORCID 0000-0003-3108-238X
Martina CebovaInstitute of Normal and Pathological Physiology, Centre of Experimental Medicine, Slovak Academy of Sciences, 841 04 Bratislava, Slovakia.ORCID 0000-0003-0132-670X
John D HendersonNovo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, DK-2200 Copenhagen, Denmark.ORCID 0000-0001-8546-1655
Andrej BartaInstitute of Normal and Pathological Physiology, Centre of Experimental Medicine, Slovak Academy of Sciences, 841 04 Bratislava, Slovakia.
Sona CacanyiovaInstitute of Normal and Pathological Physiology, Centre of Experimental Medicine, Slovak Academy of Sciences, 841 04 Bratislava, Slovakia.ORCID 0000-0003-0483-7468

Funding

Scientific Grant Agency of the Ministry of Education, Science, Research, and Sport of the Slovak Republic VEGA 2//0147/22Slovak Research and Development Agency APVV-20-0421Slovak Research and Development Agency SK-CZ-RD-21-0102
6 · The paper itself

Abstract

BACKGROUND/

objectivesMetabolic syndrome is one of the leading causes of mortality worldwide, with high-fat diet (HFD) intake being a significant driving force. Despite long-term research, new interventions are still being sought to improve cardiovascular disorders associated with metabolic syndrome.

methodsTo explore the therapeutic potential of a slow-releasing H

resultsHFD administration induced cardiac remodeling, increased adiposity, and decreased adrenergic contractility in both TAs and MAs. Moreover, although high-fat intake improved TAs relaxation, it decreased aortic protein expression of endothelial NO synthase and the involvement of NO in vasoactive responses of both TAs and MAs. In addition, protein expression of inducible NOS and tumor necrosis factor alpha (TNFα) in aortas was increased, as were plasma levels of chemerin, which has been proposed as a possible link among metabolic and vascular disorders and inflammation. Treatment with GYY-4137 reduced sBP, improved relaxation of the MAs, partially restored the contractility of the TAs, generally restored NO signaling, and decreased the protein expression of the inducible NOS and TNFα, as well as plasma chemerin levels.

conclusionsA slow H

Indexed as

GYY-4137high-fat diethydrogen sulfidespontaneously hypertensive ratvascular

Identifiers

PMID40559470
PMCPMC12196443

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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.