Evidence map›Paper›PMID 30026406›Full record

ArticleAging2018

Mitochondria-targeted hydrogen sulfide attenuates endothelial senescence by selective induction of splicing factors

Eva Latorre, Roberta Torregrossa, Mark E Wood, Matthew Whiteman, Lorna W Harries

Open access · greenAbstract read
In one paragraph

Article in Aging, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Senotherapy for chronic lung disease.Pharmacological reviews · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Cellular Senescence, Inflammation, and Cancer in the Gastrointestinal Tract.International journal of molecular sciences · 2023
    Review
  19. Article
  20. Review
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 1 institution in 1 country.

Eva LatorreUniversity of Exeter Medical School, University of Exeter, UK.
Roberta TorregrossaUniversity of Exeter Medical School, University of Exeter, UK.
Mark E WoodCollege of Life and Environmental Sciences, University of Exeter, UK.
Matthew WhitemanUniversity of Exeter Medical School, University of Exeter, UK.
Lorna W HarriesUniversity of Exeter Medical School, University of Exeter, UK.
University of Exeter · GB

Funding

Medical Research Council MC_PC_15047Medical Research Council MR/M022706/1Medical Research Council MR/S002626/1The Dunhill Medical Trust R386/1114
6 · The paper itself

Abstract

Cellular senescence is a key driver of ageing, influenced by age-related changes to the regulation of alternative splicing. Hydrogen sulfide (H

Indexed as

Cell LineCellular SenescenceEpithelial CellsGene Expression RegulationHeterogeneous-Nuclear Ribonucleoprotein DHeterogeneous Nuclear Ribonucleoprotein D0HumansHydrogen SulfideMorpholinesOrganophosphorus CompoundsOrganothiophosphorus CompoundsRNA Splicing FactorsSerine-Arginine Splicing FactorsThionesTranscriptomeAP39 compoundGYY 4137Heterogeneous-Nuclear Ribonucleoprotein DHeterogeneous Nuclear Ribonucleoprotein D0HNRNPD protein, humanHydrogen SulfideMorpholinesOrganophosphorus CompoundsOrganothiophosphorus CompoundsRNA Splicing FactorsSerine-Arginine Splicing FactorsSRSF2 protein, humanThionesAP123AP39HS 2mitochondria-targetingpersulfideperthiolRT01senescencesplicing factors

Identifiers

PMID30026406
PMCPMC6075431
OpenAlexW2883771213

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.