Evidence map›Paper›PMID 27138707›Full record

ArticleEuropean journal of pharmacology2016

Cystathionine-γ lyase-derived hydrogen sulfide mediates the cardiovascular protective effects of moxonidine in diabetic rats.

Shaimaa S El-Sayed, Mohamed N M Zakaria, Rasha H Abdel-Ghany, Abdel A Abdel-Rahman

Abstract read
In one paragraph

Article in European journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Circulating Hydrogen Sulfide (HJournal of clinical medicine · 2021
    Article
  4. Article
  5. Effects of endogenous HMolecular and cellular biochemistry · 2021
    Article
  6. Review
  7. Hydrogen Sulfide Plays an Important Role in Diabetic Cardiomyopathy.Frontiers in cell and developmental biology · 2021
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Restoration of Rostral Ventrolateral Medulla Cystathionine-The Journal of pharmacology and experimental therapeutics · 2018
    Article
  15. Review
  16. 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

4 authors at 2 institutions in 2 countries.

Shaimaa S El-SayedDepartment of Pharmacology and Toxicology, Brody School of Medicine, East Carolina University, Greenville, NC 27834, USA. Electronic address: shamy_samy84@yahoo.com.
Mohamed N M ZakariaDepartment of Pharmacology and Toxicology, Zagazig University, Zagazig, Egypt.
Rasha H Abdel-GhanyDepartment of Pharmacology and Toxicology, Zagazig University, Zagazig, Egypt.
Abdel A Abdel-RahmanDepartment of Pharmacology and Toxicology, Brody School of Medicine, East Carolina University, Greenville, NC 27834, USA. Electronic address: abdelrahmana@ecu.edu.
East Carolina University · USZagazig University · EG

Funding

Sex/estrogen-dependent vulnerability to alcohol-evoked cardiotoxicity: Role of circadian rhythm regulated enzymesR01AA014441 · NIAAA · EAST CAROLINA UNIVERSITY · PI ABDEL-RAHMAN, ABDEL A · 2004 to 2022
$5.2M
NIAAA NIH HHS R01 AA014441
6 · The paper itself

Abstract

Blunted cystathionine-γ lyase (CSE) activity (reduced endogenous H2S-level) is implicated in hypertension and myocardial dysfunction in diabetes. Here, we tested the hypothesis that CSE derived H2S mediates the cardiovascular protection conferred by the imidazoline I1 receptor agonist moxonidine in a diabetic rat model. We utilized streptozotocin (STZ; 55mg/kg i.p) to induce diabetes in male Wistar rats. Four weeks later, STZ-treated rats received vehicle, moxonidine (2 or 6mg/kg; gavage), CSE inhibitor DL-propargylglycine, (37.5mg/kg i.p) or DL-propargylglycine with moxonidine (6mg/kg) for 3 weeks. Moxonidine improved the glycemic state, and reversed myocardial hypertrophy, hypertension and baroreflex dysfunction in STZ-treated rats. Ex vivo studies revealed that STZ caused reductions in CSE expression/activity, H2S and nitric oxide (NO) levels and serum adiponectin and elevations in myocardial imidazoline I1 receptor expression, p38 and extracellular signal-regulated kinase, ERK1/2, phosphorylation and lipid peroxidation (expressed as malondialdehyde). Moxonidine reversed these biochemical responses, and suppressed the expression of death associated protein kinase-3. Finally, pharmacologic CSE inhibition (DL-propargylglycine) abrogated the favorable cardiovascular, glycemic and biochemical responses elicited by moxonidine. These findings present the first evidence for a mechanistic role for CSE derived H2S in the glycemic control and in the favorable cardiovascular effects conferred by imidazoline I1 receptor activation (moxonidine) in a diabetic rat model.

Indexed as

AdiponectinAlkynesAnimalsBaroreflexBlood GlucoseBody WeightCardiotonic AgentsCystathionine gamma-LyaseDiabetes Mellitus, ExperimentalGene Expression Regulation, EnzymologicGlycineHydrogen SulfideHypertrophyImidazolesMaleMyocardiumAdiponectinAlkynesBlood GlucoseCardiotonic AgentsCystathionine gamma-LyaseGlycineHydrogen SulfideImidazolesmoxonidinepropargylglycineCystathionine-γ lyaseDiabetesDL-propargylglycine (PubChem CID: 95575)Hydrogen SulfideHypertensionImidazoline I(1) receptor, moxonidinemoxonidine (PubChem CID: 4810)Myocardial dysfunctionstreptozotocin (PubChem CID: 29327)

Identifiers

PMID27138707
PMCPMC4893977
OpenAlexW2343595758

What OpenQuestion holds

Textmetadata
LicenceTDM
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.