Evidence map›Paper›PMID 22419888›Full record

ArticleInternational journal of biological sciences2012

Hydrogen sulfide mitigates cardiac remodeling during myocardial infarction via improvement of angiogenesis.

Natia Qipshidze, Naira Metreveli, Paras K Mishra, David Lominadze, Suresh C Tyagi

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
6.8field-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

64 citing papers in PubMed, 102 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Clinical Potential of Hydrogen Sulfide in Peripheral Arterial Disease.International journal of molecular sciences · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Endostatin in Renal and Cardiovascular Diseases.Kidney diseases (Basel, Switzerland) · 2021
    Review
  19. Review
  20. Article

4 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 2 countries.

Natia QipshidzeDepartment of Physiology, University of Louisville School of Medicine, Louisville, Kentucky 40202, USA. n0qips01@louisville.edu
Naira Metreveli
Paras K Mishra
David Lominadze
Suresh C Tyagi
University of Louisville Hospital · USLaboratoire d’immunologie intégrative du cancer · FRUniversity of Louisville · US

Funding

Reversing diabetic muscle myopathy by exercise and exosomesR01HL074185 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TYAGI, SURESH C. · 2003 to 2018
$5.7M
Mechanism of Vascular Remodeling in HyperhomocysteinemiaR01HL071010 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI TYAGI, SURESH C. · 2002 to 2010
$2.7M
Fibronogen-Induced Vasconstriction during HypertensionR01HL080394 · NHLBI · UNIVERSITY OF LOUISVILLE · PI LOMINADZE, DAVID · 2007 to 2011
$2.1M
Implications of Endothelial-Myocyte Uncoupling in Cardiac ArrhythmiaR01HL088012 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TYAGI, SURESH C. · 2007 to 2010
$1.5M
NHLBI NIH HHS HL-71010NHLBI NIH HHS HL-74185NHLBI NIH HHS HL-80394NHLBI NIH HHS HL-88012NHLBI NIH HHS R01 HL071010NHLBI NIH HHS R01 HL074185NHLBI NIH HHS R01 HL080394NHLBI NIH HHS R01 HL088012
6 · The paper itself

Abstract

Exogenous hydrogen sulfide (H2S) leads to down-regulation of inflammatory responses and provides myocardial protection during acute ischemia/reperfusion injury; however its role during chronic heart failure (CHF) due to myocardial infarction (MI) is yet to be unveiled. We previously reported that H2S inhibits antiangiogenic factors such, as endostatin and angiostatin, but a little is known about its effect on parstatin (a fragment of proteinase-activated receptor-1, PAR-1). We hypothesize that H2S inhibits parstatin formation and promotes VEGF activation, thus promoting angiogenesis and significantly limiting the extent of MI injury. To verify this hypothesis MI was created in 12 week-old male mice by ligation of left anterior descending artery (LAD). Sham surgery was performed except LAD ligation. After the surgery mice were treated with sodium hydrogen sulfide (30 μmol/l NaHS, a donor for H2S, in drinking water) for 4 weeks. The LV tissue was analyzed for VEGF, flk-1 and flt-1, endostatin, angiostatin and parstatin. The expression of VEGF, flk-1 and flt-1 were significantly increased in treated mice while the level of endostatin, angiostatin and parstatin were decreased compared to in untreated mice. The echocardiography in mice treated with H2S showed the improvement of heart function compared to in untreated mice. The X-ray and Doppler blood flow measurements showed enhancement of cardiac-angiogenesis in mice treated with H2S. This observed cytoprotection was associated with an inhibition of anti-angiogenic proteins and stimulation of angiogenic factors. We established that administration of H2S at the time of MI ameliorated infarct size and preserved LV function during development of MI in mice. These results suggest that H2S is cytoprotective and angioprotective during evolution of MI.

Indexed as

AngiostatinsAnimalsBlotting, WesternEchocardiographyEndostatinsHydrogen SulfideImmunohistochemistryMaleMiceMicroscopy, ConfocalMyocardial InfarctionNeovascularization, PhysiologicReverse Transcriptase Polymerase Chain ReactionVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2AngiostatinsEndostatinsHydrogen SulfideVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2angiostatinendostatinflk-1flt-1Hydrogen sulfideparstatin Myocardial infarctionVEGF

Identifiers

PMID22419888
PMCPMC3303169
OpenAlexW2113994981

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.