Evidence map›Paper›PMID 19955410›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Hydrogen sulfide is an endogenous stimulator of angiogenesis.

Andreas Papapetropoulos, Anastasia Pyriochou, Zaid Altaany, Guangdong Yang, Antonia Marazioti, Zongmin Zhou, Mark G Jeschke, Ludwik K Branski, David N Herndon, Rui Wang and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 353 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
353citing papers in PubMed, 1 pooled it
18.2field-weighted citation impact, top 1% 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

353 citing papers in PubMed, 1 synthesis or guideline pooled it, 856 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
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  5. Article
  6. Article
  7. HCellular & molecular biology letters · 2026
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  8. Brain-Derived Cystathionine β-Synthase-Generated HCurrent issues in molecular biology · 2026
    Article
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  11. Article
  12. Article
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  16. HJournal of nanobiotechnology · 2025
    Article
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  19. Targeting macro- and micro-nutrient regulation of HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  20. Review

293 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

11 authors at 5 institutions in 3 countries.

Andreas PapapetropoulosLaboratory of Molecular Pharmacology, Department of Pharmacy, University of Patras 265 04 Rio Patras, Patras, Greece.
Anastasia Pyriochou
Zaid Altaany
Guangdong Yang
Antonia Marazioti
Zongmin Zhou
Mark G Jeschke
Ludwik K Branski
David N Herndon
Rui Wang
Csaba Szabó
Lakehead University · CAThe University of Texas Medical Branch at Galveston · USUniversity of Patras · GRJohns Hopkins Medicine · USNational and Kapodistrian University of Athens · GR

Funding

POLY (ADP RIBOSE) SYNTHETASE AND PEROXYNITRITE INDUCED CR01GM060915 · NIGMS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SZABO, CSABA · 1999 to 2009
$1.9M
CIHRNIGMS NIH HHS R01 GM060915
6 · The paper itself

Abstract

The goal of the current study was to investigate the role of exogenous and endogenous hydrogen sulfide (H(2)S) on neovascularization and wound healing in vitro and in vivo. Incubation of endothelial cells (ECs) with H(2)S enhanced their angiogenic potential, evidenced by accelerated cell growth, migration, and capillary morphogenesis on Matrigel. Treatment of chicken chorioallantoic membranes (CAMS) with H(2)S increased vascular length. Exposure of ECs to H(2)S resulted in increased phosphorylation of Akt, ERK, and p38. The K(ATP) channel blocker glibenclamide or the p38 inhibitor SB203580 abolished H(2)S-induced EC motility. Since glibenclamide inhibited H(2)S-triggered p38 phosphorylation, we propose that K(ATP) channels lay upstream of p38 in this process. When CAMs were treated with H(2)S biosynthesis inhibitors dl-propylargylglycine or beta-cyano-L-alanine, a reduction in vessel length and branching was observed, indicating that H(2)S serves as an endogenous stimulator of the angiogenic response. Stimulation of ECs with vascular endothelial growth factor (VEGF) increased H(2)S release, while pharmacological inhibition of H(2)S production or K(ATP) channels or silencing of cystathionine gamma-lyase (CSE) attenuated VEGF signaling and migration of ECs. These results implicate endothelial H(2)S synthesis in the pro-angiogenic action of VEGF. Aortic rings isolated from CSE knockout mice exhibited markedly reduced microvessel formation in response to VEGF when compared to wild-type littermates. Finally, in vivo, topical administration of H(2)S enhanced wound healing in a rat model, while wound healing was delayed in CSE(-/-) mice. We conclude that endogenous and exogenous H(2)S stimulates EC-related angiogenic properties through a K(ATP) channel/MAPK pathway.

Indexed as

ApoptosisCells, CulturedEndothelium, VascularHumansHydrogen SulfideNeovascularization, PhysiologicSignal TransductionWound HealingHydrogen Sulfide

Identifiers

PMID19955410
PMCPMC2799889
OpenAlexW2035143128

What OpenQuestion holds

Textmetadata
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.