Evidence map›Paper›PMID 26078813›Full record

ArticleOxidative medicine and cellular longevity2015

Hydrogen Sulfide Donor GYY4137 Protects against Myocardial Fibrosis.

Guoliang Meng, Jinbiao Zhu, Yujiao Xiao, Zhengrong Huang, Yuqing Zhang, Xin Tang, Liping Xie, Yu Chen, Yongfeng Shao, Albert Ferro and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.6field-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

41 citing papers in PubMed, 88 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. A Slow Hydrogen Sulfide Donor GYY-4137 Partially Improves Vascular Function in Spontaneously Hypertensive Rats Fed a High-Fat Diet.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Article
  5. Review
  6. Review
  7. Review
  8. Exogenous hydrogen sulfide attenuates hyperoxia effects on neonatal mouse airways.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  9. Article
  10. Article
  11. Vasoactive Effects of Chronic Treatment with Fructose and Slow-Releasing HInternational journal of molecular sciences · 2022
    Article
  12. Unmet needs in glaucoma therapy: The potential role of hydrogen sulfide and its delivery strategies.Journal of controlled release : official journal of the Controlled Release Society · 2022
    Review
  13. Hydrogen Sulfide Biology and Its Role in Cancer.Molecules (Basel, Switzerland) · 2022
    Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
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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

13 authors at 7 institutions in 4 countries.

Guoliang MengKey Laboratory of Cardiovascular Disease and Molecular Intervention, Atherosclerosis Research Centre, Nanjing Medical University, Nanjing 210029, China ; Department of Pharmacology, School of Pharmacy, Nantong University, Nantong 226001, China.
Jinbiao ZhuAoyong Hospital, Zhangjiagang 215600, China.
Yujiao XiaoKey Laboratory of Cardiovascular Disease and Molecular Intervention, Atherosclerosis Research Centre, Nanjing Medical University, Nanjing 210029, China ; Department of Pathology, Jincheng People's Hospital, Jincheng 048000, China.
Zhengrong HuangDepartment of Cardiology, The First Affiliated Hospital of Xiamen University, Xiamen 361003, China.
Yuqing ZhangDepartment of Cardiology, The Affiliated Jiangning Hospital of Nanjing Medical University, Nanjing 211100, China.
Xin TangKey Laboratory of Cardiovascular Disease and Molecular Intervention, Atherosclerosis Research Centre, Nanjing Medical University, Nanjing 210029, China.
Liping XieKey Laboratory of Cardiovascular Disease and Molecular Intervention, Atherosclerosis Research Centre, Nanjing Medical University, Nanjing 210029, China.
Yu ChenDepartment of Anesthesia, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Yongfeng ShaoDepartment of Thoracic and Cardiac Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Albert FerroCardiovascular Division, Department of Clinical Pharmacology, British Heart Foundation Centre of Research Excellence, Faculty of Life Sciences and Medicine, King's College London, London SE1 9NH, UK.
Rui WangDepartment of Biology, Lakehead University, Thunder Bay, ON, Canada P7B 5E1.
Philip K MooreDepartment of Pharmacology, National University of Singapore, Singapore 117597.
Yong JiKey Laboratory of Cardiovascular Disease and Molecular Intervention, Atherosclerosis Research Centre, Nanjing Medical University, Nanjing 210029, China.
Nanjing Medical University · CNFirst Affiliated Hospital of Xiamen University · CNKing's College London · GBLakehead University · CANantong University · CNNational University of Singapore · SGZhangjiagang First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hydrogen sulfide (H2S) is a gasotransmitter which regulates multiple cardiovascular functions. However, the precise roles of H2S in modulating myocardial fibrosis in vivo and cardiac fibroblast proliferation in vitro remain unclear. We investigated the effect of GYY4137, a slow-releasing H2S donor, on myocardial fibrosis. Spontaneously hypertensive rats (SHR) were administrated with GYY4137 by intraperitoneal injection daily for 4 weeks. GYY4137 decreased systolic blood pressure and inhibited myocardial fibrosis in SHR as evidenced by improved cardiac collagen volume fraction (CVF) in the left ventricle (LV), ratio of perivascular collagen area (PVCA) to lumen area (LA) in perivascular regions, reduced hydroxyproline concentration, collagen I and III mRNA expression, and cross-linked collagen. GYY4137 also inhibited angiotensin II- (Ang II-) induced neonatal rat cardiac fibroblast proliferation, reduced the number of fibroblasts in S phase, decreased collagen I and III mRNA expression and protein synthesis, attenuated oxidative stress, and suppressed α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1) expression as well as Smad2 phosphorylation. These results indicate that GYY4137 improves myocardial fibrosis perhaps by a mechanism involving inhibition of oxidative stress, blockade of the TGF-β1/Smad2 signaling pathway, and decrease in α-SMA expression in cardiac fibroblasts.

Indexed as

ActinsAngiotensin IIAnimalsBlood PressureCell ProliferationCells, CulturedCollagen Type ICollagen Type IIFibroblastsHeartHeart VentriclesHydroxyprolineMaleMorpholinesMyocardiumOrganothiophosphorus CompoundsActa2 protein, ratActinsAngiotensin IICollagen Type ICollagen Type IIGYY 4137HydroxyprolineMorpholinesOrganothiophosphorus CompoundsReactive Oxygen SpeciesSmad2 ProteinSmad2 protein, ratTransforming Growth Factor beta1

Identifiers

PMID26078813
PMCPMC4442292
OpenAlexW1593096883

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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.