Evidence map›Paper›PMID 32980857›Full record

ArticleCell death & disease2020

Endothelin 1-induced retinal ganglion cell death is largely mediated by JUN activation.

Olivia J Marola, Stephanie B Syc-Mazurek, Gareth R Howell, Richard T Libby

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. IL1A enhances TNF-induced retinal ganglion cell death.Frontiers in aging neuroscience · 2026
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  14. Multiple Sclerosis: Inflammatory and Neuroglial Aspects.Current issues in molecular biology · 2023
    Review
  15. Review
  16. Article
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  18. Damage-Associated Molecular Patterns (DAMPs) in Retinal Disorders.International journal of molecular sciences · 2022
    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

4 authors at 2 institutions in 1 country.

Olivia J MarolaDepartment of Ophthalmology, Flaum Eye Institute, University of Rochester Medical Center, Rochester, NY, USA.ORCID http://orcid.org/0000-0002-0078-6088
Stephanie B Syc-MazurekDepartment of Ophthalmology, Flaum Eye Institute, University of Rochester Medical Center, Rochester, NY, USA.
Gareth R HowellThe Jackson Laboratory, 600 Main Street, Bar Harbor, ME, USA.
Richard T LibbyDepartment of Ophthalmology, Flaum Eye Institute, University of Rochester Medical Center, Rochester, NY, USA. richard_libby@urmc.rochester.edu.ORCID http://orcid.org/0000-0003-2844-7632
University of Rochester Medical Center · USJackson Laboratory · US

Funding

University of Rochester Mentoring Environment: Nurturing Training Opportunities in Research (UR-MENTOR)T32GM007356 · NIGMS · UNIVERSITY OF ROCHESTER · PI O'BANION, M. KERRY · 1985 to 2023
$15.1M
VISUAL SCIENCET32EY007125 · NEI · UNIVERSITY OF ROCHESTER · PI Krystel R Huxlin, Duje Tadin · 1990 to 2026
$7.1M
Cell Death Pathways in Glaucomatous NeurodegenerationR01EY018606 · NEI · UNIVERSITY OF ROCHESTER · PI JOHN, SIMON W, LIBBY, RICHARD T · 2008 to 2023
$5.8M
Cell specific roles of the endothelin system in glaucoma-relevant retinal ganglion cell deathR01EY027701 · NEI · UNIVERSITY OF ROCHESTER · PI HOWELL, GARETH R, LIBBY, RICHARD T · 2017 to 2021
$2.7M
Endothelin Signaling in Glaucomatous NeurodegenerationF31EY030739 · NEI · UNIVERSITY OF ROCHESTER · PI MAROLA, OLIVIA JOYCE · 2020 to 2021
$85k
NEI NIH HHS F31 EY030739NEI NIH HHS R01 EY018606NEI NIH HHS R01 EY027701NEI NIH HHS T32 EY007125NIGMS NIH HHS T32 GM007356
6 · The paper itself

Abstract

Glaucoma is a neurodegenerative disease characterized by loss of retinal ganglion cells (RGCs), the output neurons of the retina. Multiple lines of evidence show the endothelin (EDN, also known as ET) system is important in glaucomatous neurodegeneration. To date, the molecular mechanisms within RGCs driving EDN-induced RGC death have not been clarified. The pro-apoptotic transcription factor JUN (the canonical target of JNK signaling) and the endoplasmic reticulum stress effector and transcription factor DNA damage inducible transcript 3 (DDIT3, also known as CHOP) have been shown to act downstream of EDN receptors. Previous studies demonstrated that JUN and DDIT3 were important regulators of RGC death after glaucoma-relevant injures. Here, we characterized EDN insult in vivo and investigated the role of JUN and DDIT3 in EDN-induced RGC death. To accomplish this, EDN1 ligand was intravitreally injected into the eyes of wildtype, Six3-cre

Indexed as

AnimalsCell DeathDisease Models, AnimalEndothelin-1Genes, junGlaucomaHumansMiceMice, Inbred C57BLRetinal Ganglion CellsEndothelin-1

Identifiers

PMID32980857
PMCPMC7519907
OpenAlexW3089037475

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.