Evidence map›Paper›PMID 25397776›Full record

ArticlePloS one2014

Anti-atherogenic effect of hydrogen sulfide by over-expression of cystathionine gamma-lyase (CSE) gene.

Sau Ha Cheung, Wai Kei Kwok, Ka Fai To, James Yun Wong Lau

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.7field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 52 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Diabetic Nephropathy and Gaseous Modulators.Antioxidants (Basel, Switzerland) · 2023
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Reactive Sulfur Species: A New Redox Player in Cardiovascular Pathophysiology.Arteriosclerosis, thrombosis, and vascular biology · 2020
    Article
  11. Review
  12. Review
  13. Cystathionine γ-Lyase Modulates Flow-Dependent Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Article
  14. Hydrogen Sulfide (HFrontiers in pharmacology · 2018
    Review
  15. Article
  16. Review
  17. Vascular biology of hydrogen sulfide.American journal of physiology. Cell physiology · 2017
    Review
  18. HCellular and molecular life sciences : CMLS · 2017
    Review
  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

4 authors at 1 institution in 1 country.

Sau Ha CheungDepartment of Surgery, Faculty of Medicine, the Chinese University of Hong Kong, Hong Kong SAR, People's Republic of China.
Wai Kei KwokDepartment of Surgery, Faculty of Medicine, the Chinese University of Hong Kong, Hong Kong SAR, People's Republic of China.
Ka Fai ToDepartment of Anatomical and Cellular Pathology, Faculty of Medicine, the Chinese University of Hong Kong, Hong Kong SAR, People's Republic of China.
James Yun Wong LauDepartment of Surgery, Faculty of Medicine, the Chinese University of Hong Kong, Hong Kong SAR, People's Republic of China.
Chinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hydrogen sulfide (H2S) is an important gaseous signaling molecule that functions in physiological and pathological conditions, such as atherosclerosis. H2S dilates vessels and therefore has been suggested as an anti-atherogenic molecule. Since cystathionine gamma-lyase (CSE) enzyme is responsible for producing H2S in the cardiovascular system, we hypothesized that up-regulation of CSE expression in vivo with preservation of H2S bioactivity can slow down plaque formation and, can serve as a therapeutic strategy against atherosclerosis. In this study, C57BL/6 wild type mice (WT), ApoE knockout mice (KO) and transgenic ApoE knockout mice overexpressing CSE (Tg/KO) at four weeks of age were weaned. They were then fed with either normal or atherogenic diet for 12 weeks. At week 16, serial plasma lipid levels, body weight, and blood pressure were measured prior to euthanization of the mice and the size of atherosclerotic plaques at their aortic roots was measured. Tg/KO mice showed an increase in endogenous H2S production in aortic tissue, reduced atherosclerotic plaque sizes and attenuation in plasma lipid profiles. We also showed an up-regulation in plasma glutathionine peroxidase that could indicate reduced oxidative stress. Furthermore, there was an increase in expression of p-p53 and down regulation of inflammatory nuclear factor-kappa B (NF-κB) in aorta. To conclude, alteration of endogenous H2S by CSE gene activation was associated with reduced atherosclerosis in ApoE-deficient mice. Up-regulation of CSE/H2S pathway attenuates atherosclerosis and this would be a potential target for therapeutic intervention against its formation.

Indexed as

AdiponectinAnimalsAortaApolipoproteins EAtherosclerosisBlood PressureBody WeightCystathionine gamma-LyaseDown-RegulationGlutathione PeroxidaseHydrogen SulfideLeptinLipidsMiceMice, Inbred C57BLMice, KnockoutAdiponectinApolipoproteins ECystathionine gamma-LyaseGlutathione PeroxidaseHydrogen SulfideLeptinLipidsNF-kappa BTumor Suppressor Protein p53

Identifiers

PMID25397776
PMCPMC4232559
OpenAlexW1992999472

What OpenQuestion holds

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LicenceCC BY
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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.