Evidence map›Paper›PMID 23991830›Full record

ReviewBritish journal of pharmacology2014

Regulation of mitochondrial bioenergetic function by hydrogen sulfide. Part I. Biochemical and physiological mechanisms.

Csaba Szabo, Céline Ransy, Katalin Módis, Mireille Andriamihaja, Baptiste Murghes, Ciro Coletta, Gabor Olah, Kazunori Yanagi, Frédéric Bouillaud

Open access · greenAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 234 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
234citing papers in PubMed, 1 pooled it
13.8field-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

234 citing papers in PubMed, 1 synthesis or guideline pooled it, 434 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. A Paradigm Shift of HCurrent issues in molecular biology · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Changes in the brain [NADFrontiers in aging neuroscience · 2026
    Review
  18. Hydrogen Sulfide Signaling in Neurodegenerative Movement Disorders.Handbook of experimental pharmacology · 2026
    Review
  19. Article
  20. Article

174 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

9 authors at 3 institutions in 2 countries.

Csaba SzaboDepartment of Anesthesiology, University of Texas Medical Branch, Galveston, TX, USA.
Céline Ransy
Katalin Módis
Mireille Andriamihaja
Baptiste Murghes
Ciro Coletta
Gabor Olah
Kazunori Yanagi
Frédéric Bouillaud
The University of Texas Medical Branch at Galveston · USInstitut Cochin · FRAgroParisTech · FR

Funding

Project 9: The role of androgen/corticosteroid in fat, muscle and glucose metabolism of burn victimsP50GM060338 · NIGMS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI SZABO, CSABA · 2000 to 2017
$24.2M
Regulation of cellular bioenergetics by hydrogen sulfideR01GM107846 · NIGMS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI SZABO, CSABA · 2014 to 2017
$1.2M
NIGMS NIH HHS P50 GM060338NIGMS NIH HHS P50GM060338NIGMS NIH HHS R01 GM107846
6 · The paper itself

Abstract

Until recently, hydrogen sulfide (H2 S) was exclusively viewed a toxic gas and an environmental hazard, with its toxicity primarily attributed to the inhibition of mitochondrial Complex IV, resulting in a shutdown of mitochondrial electron transport and cellular ATP generation. Work over the last decade established multiple biological regulatory roles of H2 S, as an endogenous gaseous transmitter. H2 S is produced by cystathionine γ-lyase (CSE), cystathionine β-synthase (CBS) and 3-mercaptopyruvate sulfurtransferase (3-MST). In striking contrast to its inhibitory effect on Complex IV, recent studies showed that at lower concentrations, H2 S serves as a stimulator of electron transport in mammalian cells, by acting as a mitochondrial electron donor. Endogenous H2 S, produced by mitochondrially localized 3-MST, supports basal, physiological cellular bioenergetic functions; the activity of this metabolic support declines with physiological aging. In specialized conditions (calcium overload in vascular smooth muscle, colon cancer cells), CSE and CBS can also associate with the mitochondria; H2 S produced by these enzymes, serves as an endogenous stimulator of cellular bioenergetics. The current article overviews the biochemical mechanisms underlying the stimulatory and inhibitory effects of H2 S on mitochondrial function and cellular bioenergetics and discusses the implication of these processes for normal cellular physiology. The relevance of H2 S biology is also discussed in the context of colonic epithelial cell physiology: colonocytes are exposed to high levels of sulfide produced by enteric bacteria, and serve as a metabolic barrier to limit their entry into the mammalian host, while, at the same time, utilizing it as a metabolic 'fuel'.

Indexed as

AnimalsCell RespirationColonElectron TransportEnergy MetabolismEpithelial CellsGasotransmittersHumansHydrogen SulfideMitochondriaModels, BiologicalGasotransmittersHydrogen Sulfide3-mercaptopyruvate sulfurtransferasebioenergeticsblood vesselscysteinecytochrome c oxidasefree radicalsgasotransmittersmitochondrial electron transportnitric oxidesuperoxide

Identifiers

PMID23991830
PMCPMC3976625
OpenAlexW1655368476

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.