Evidence map›Paper›PMID 28678794›Full record

ArticlePLoS medicine2017

Ammonium tetrathiomolybdate following ischemia/reperfusion injury: Chemistry, pharmacology, and impact of a new class of sulfide donor in preclinical injury models.

Alex Dyson, Felipe Dal-Pizzol, Giovanni Sabbatini, Anna B Lach, Federica Galfo, Juliano Dos Santos Cardoso, Bruna Pescador Mendonça, Iain Hargreaves, Bernardo Bollen Pinto, Daniel I Bromage and 4 more

Open access · goldAbstract read
In one paragraph

Article in PLoS medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 3 pooled it
2.8field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 3 syntheses or guidelines pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. The Yin and Yang of copper in cardiovascular health and disease.Molecular and cellular biochemistry · 2026
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Cuproptosis and copper deficiency in ischemic vascular injury and repair.Apoptosis : an international journal on programmed cell death · 2024
    Review
  12. Mechanisms of cuproptosis and its relevance to distinct diseases.Apoptosis : an international journal on programmed cell death · 2024
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. HBiomolecules · 2022
    Review
  18. 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

14 authors at 4 institutions in 2 countries.

Alex DysonBloomsbury Institute for Intensive Care Medicine, Division of Medicine, University College London, London, United Kingdom.ORCID http://orcid.org/0000-0001-8334-9432
Felipe Dal-PizzolBloomsbury Institute for Intensive Care Medicine, Division of Medicine, University College London, London, United Kingdom.
Giovanni SabbatiniBloomsbury Institute for Intensive Care Medicine, Division of Medicine, University College London, London, United Kingdom.
Anna B LachBloomsbury Institute for Intensive Care Medicine, Division of Medicine, University College London, London, United Kingdom.
Federica GalfoBloomsbury Institute for Intensive Care Medicine, Division of Medicine, University College London, London, United Kingdom.ORCID http://orcid.org/0000-0002-8786-8042
Juliano Dos Santos CardosoLaboratory of Experimental Pathophysiology, University of Southern Santa Catarina, Criciúma, Brazil.
Bruna Pescador MendonçaLaboratory of Experimental Pathophysiology, University of Southern Santa Catarina, Criciúma, Brazil.
Iain HargreavesDepartment of Molecular Neuroscience, Institute of Neurology, University College London, London, United Kingdom.
Bernardo Bollen PintoBloomsbury Institute for Intensive Care Medicine, Division of Medicine, University College London, London, United Kingdom.
Daniel I BromageHatter Cardiovascular Institute, University College London, London, United Kingdom.
John F MartinBloomsbury Institute for Intensive Care Medicine, Division of Medicine, University College London, London, United Kingdom.
Kevin P MooreInstitute for Liver and Digestive Health, University College London, London, United Kingdom.
Martin FeelischClinical and Experimental Sciences, Faculty of Medicine, Southampton General Hospital and Institute for Life Sciences, University of Southampton, Southampton, United Kingdom.
Mervyn SingerBloomsbury Institute for Intensive Care Medicine, Division of Medicine, University College London, London, United Kingdom.ORCID http://orcid.org/0000-0002-1042-6350
Bury College · GBUniversity College London · GBSouthampton General Hospital · GBUniversity of Messina · IT

Funding

Medical Research Council G1001340Medical Research Council G1001536Medical Research Council MR/L002043/1Medical Research Council MR/N007085/1
6 · The paper itself

Abstract

backgroundEarly revascularization of ischemic organs is key to improving outcomes, yet consequent reperfusion injury may be harmful. Reperfusion injury is largely attributed to excess mitochondrial production of reactive oxygen species (ROS). Sulfide inhibits mitochondria and reduces ROS production. Ammonium tetrathiomolybdate (ATTM), a copper chelator, releases sulfide in a controlled and novel manner, and may offer potential therapeutic utility. METHODS AND

findingsIn vitro, ATTM releases sulfide in a time-, pH-, temperature-, and thiol-dependent manner. Controlled sulfide release from ATTM reduces metabolism (measured as oxygen consumption) both in vivo in awake rats and ex vivo in skeletal muscle tissue, with a superior safety profile compared to standard sulfide generators. Given intravenously at reperfusion/resuscitation to rats, ATTM significantly reduced infarct size following either myocardial or cerebral ischemia, and conferred survival benefit following severe hemorrhage. Mechanistic studies (in vitro anoxia/reoxygenation) demonstrated a mitochondrial site of action (decreased MitoSOX fluorescence), where the majority of damaging ROS is produced.

conclusionsThe inorganic thiometallate ATTM represents a new class of sulfide-releasing drugs. Our findings provide impetus for further investigation of this compound as a novel adjunct therapy for reperfusion injury.

Indexed as

AnimalsChelating AgentsMaleMolybdenumRatsRats, WistarReperfusion InjuryChelating AgentsMolybdenumtetrathiomolybdate

Identifiers

PMID28678794
PMCPMC5497958
OpenAlexW2724982449

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.