Evidence map›Paper›PMID 25311168›Full record

ReviewExperimental eye research2014

Transcript profile of cellular senescence-related genes in Fuchs endothelial corneal dystrophy.

Mario Matthaei, Angela Y Zhu, Laura Kallay, Charles G Eberhart, Claus Cursiefen, Albert S Jun

Abstract readReview
In one paragraph

Review in Experimental eye research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. COL8A2 Regulates the Fate of Corneal Endothelial Cells.Investigative ophthalmology & visual science · 2020
    Article
  12. Article
  13. Article
  14. Corneal dystrophies.Nature reviews. Disease primers · 2020
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  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

6 authors.

Mario MatthaeiThe Wilmer Eye Institute, Johns Hopkins Medical Institutions, Baltimore, USA; Department of Ophthalmology, University of Cologne, Cologne, Germany; Department of Ophthalmology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Angela Y ZhuThe Wilmer Eye Institute, Johns Hopkins Medical Institutions, Baltimore, USA.
Laura KallayThe Wilmer Eye Institute, Johns Hopkins Medical Institutions, Baltimore, USA.
Charles G EberhartThe Wilmer Eye Institute, Johns Hopkins Medical Institutions, Baltimore, USA.
Claus CursiefenDepartment of Ophthalmology, University of Cologne, Cologne, Germany.
Albert S JunThe Wilmer Eye Institute, Johns Hopkins Medical Institutions, Baltimore, USA. Electronic address: aljun@jhmi.edu.

Funding

Role of unfolded protein response and COL8A2 in Fuchs corneal dystrophyR01EY019874 · NEI · JOHNS HOPKINS UNIVERSITY · PI JUN, ALBERT S · 2010 to 2014
$2.0M
NEI NIH HHS NIH EY019874NEI NIH HHS R01 EY019874
6 · The paper itself

Abstract

Fuchs endothelial corneal dystrophy (FECD) is a genetically heterogeneous disease. Hypothesizing that cellular senescence may be relevant in FECD pathogenesis, genetically undifferentiated late-onset FECD endothelial samples were analyzed to identify common changes of specific senescence-related transcripts. Total RNA was extracted from 21 FECD endothelial samples retrieved from patients undergoing lamellar keratoplasty due to clinically diagnosed end-stage FECD and from 12 endothelial samples retrieved from normal autopsy eyes. Taqman low density array (TLDA) cards were used to analyze differential expression of 89 cellular senescence-related transcripts. Result validation was performed using individual real-time PCR assays. TLDA-analysis demonstrated differential expression of 31 transcripts (fold-change >1.5; p < 0.05). Thereof, 27 showed significant up-regulation and 4 significant down-regulation. Markedly elevated mRNA-levels of the constitutively active and reactive oxygen species-generating enzyme NOX4 were found in all evaluable FECD samples. In addition, increased expression of CDKN2A and its transcriptional activators ETS1 and ARHGAP18 (SENEX) along with decreased expression of CDKN2A inhibitor ID1 were detected in FECD samples. Consistent over-expression of NOX4 in FECD endothelial samples suggests a role as pathogenic factor and as a potential new treatment target in FECD. Transcriptional up-regulation of the CDKN2A-pathway provides further evidence for increased cellular senescence in FECD endothelium.

Indexed as

ApoptosisCellular SenescenceFuchs' Endothelial DystrophyGene Expression RegulationEndothelium, CornealEye ProteinsHumansOxidative StressReactive Oxygen SpeciesReal-Time Polymerase Chain ReactionRNA, MessengerEye ProteinsReactive Oxygen SpeciesRNA, MessengerCDKN2ACellular senescenceCorneal endotheliumFuchs endothelial corneal dystrophyNOX4Oxidative stressPathogenesis

Identifiers

PMID25311168
PMCPMC4259834

What OpenQuestion holds

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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.