Evidence map›Paper›PMID 26733303›Full record

ReviewNeuroscience letters2016

Role of HDACs in optic nerve damage-induced nuclear atrophy of retinal ganglion cells.

Heather M Schmitt, Cassandra L Schlamp, Robert W Nickells

Abstract readReview
In one paragraph

Review in Neuroscience letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

27 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Retinoid X receptor agonist 9CDHRA mitigates retinal ganglion cell apoptosis and neuroinflammation in a mouse model of glaucoma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  5. Article
  6. Article
  7. Epigenetics in Glaucoma.Medicina (Kaunas, Lithuania) · 2024
    Review
  8. Dysregulation of histone deacetylases in ocular diseases.Archives of pharmacal research · 2024
    Review
  9. Article
  10. Article
  11. Review
  12. Aging Effects on Optic Nerve Neurodegeneration.International journal of molecular sciences · 2023
    Review
  13. Epigenetic Regulation of Optic Nerve Development, Protection, and Repair.International journal of molecular sciences · 2022
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. HDAC2 Regulates Glial Cell Activation in Ischemic Mouse Retina.International journal of molecular sciences · 2019
    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

3 authors at 1 institution in 1 country.

Heather M SchmittDepartment of Ophthalmology and Visual Sciences, University of Wisconsin-Madison, Madison, WI, USA.
Cassandra L SchlampDepartment of Ophthalmology and Visual Sciences, University of Wisconsin-Madison, Madison, WI, USA.
Robert W NickellsDepartment of Ophthalmology and Visual Sciences, University of Wisconsin-Madison, Madison, WI, USA. Electronic address: nickells@wisc.edu.
University of Wisconsin–Madison · US

Funding

UW Vision Research Core - Administrative CoreP30EY016665 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI ROBERT W NICKELLS · 2005 to 2026
$12.6M
The molecular mechanism of retinal ganglion cell deathR01EY012223 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI NICKELLS, ROBERT W · 2005 to 2017
$6.3M
NEI NIH HHS P30 EY016665NEI NIH HHS R01 EY012223
6 · The paper itself

Abstract

Optic neuropathies are characterized by retinal ganglion cell (RGC) death, resulting in the loss of vision. In glaucoma, the most common optic neuropathy, RGC death is initiated by axonal damage, and can be modeled by inducing acute axonal trauma through procedures such as optic nerve crush (ONC) or optic nerve axotomy. One of the early events of RGC death is nuclear atrophy, and is comprised of RGC-specific gene silencing, histone deacetylation, heterochromatin formation, and nuclear shrinkage. These early events appear to be principally regulated by epigenetic mechanisms involving histone deacetylation. Class I histone deacetylases HDACs 1, 2, and 3 are known to play important roles in the process of early nuclear atrophy in RGCs, and studies using both inhibitors and genetic ablation of Hdacs also reveal a critical role in the cell death process. Select inhibitors, such as those being developed for cancer therapy, may also provide a viable secondary treatment option for optic neuropathies.

Indexed as

ApoptosisAnimalsAtrophyDisease Models, AnimalEpigenesis, GeneticGlaucomaHistone Deacetylase InhibitorsHistone DeacetylasesHumansNerve CrushOptic Nerve DiseasesRetinal Ganglion CellsSignal TransductionHistone Deacetylase InhibitorsHistone DeacetylasesApoptosisGlaucomaHeterochromatinHistone deacetylase (HDAC)NeurodegenerationNuclear atrophyOptic nerve injuryRetinal ganglion cell

Identifiers

PMID26733303
PMCPMC5125391
OpenAlexW2210494830

What OpenQuestion holds

Textmetadata
LicenceTDM
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.