Evidence map›Paper›PMID 31301400›Full record

ReviewProgress in retinal and eye research2019

Axon injury signaling and compartmentalized injury response in glaucoma.

Stephanie B Syc-Mazurek, Richard T Libby

Open access · greenAbstract readReview
In one paragraph

Review in Progress in retinal and eye research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
10.5field-weighted citation impact, top 1% 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

68 citing papers in PubMed, 92 citations in OpenAlex.

  1. Neuroinflammation in glaucoma: a myriad of cellular pathways and players.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
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  8. Review
  9. IL1A enhances TNF-induced retinal ganglion cell death.Frontiers in aging neuroscience · 2026
    Article
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  15. Review
  16. Review
  17. 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
  18. Article
  19. Article
  20. Article

8 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Stephanie B Syc-MazurekDepartment of Ophthalmology, University of Rochester Medical Center, Rochester, NY, USA; Neuroscience Graduate Program, University of Rochester Medical Center, Rochester, NY, USA.
Richard T LibbyDepartment of Ophthalmology, University of Rochester Medical Center, Rochester, NY, USA; Department of Biomedical Genetics, University of Rochester Medical Center, Rochester, NY, USA; The Center for Visual Sciences, University of Rochester, Rochester, NY, USA. Electronic address: richard_libby@urmc.rochester.edu.
University of Rochester Medical Center · US

Funding

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
NEI NIH HHS R01 EY018606NEI NIH HHS R01 EY027701
6 · The paper itself

Abstract

Axonal degeneration is an active, highly controlled process that contributes to beneficial processes, such as developmental pruning, but also to neurodegeneration. In glaucoma, ocular hypertension leads to vision loss by killing the output neurons of the retina, the retinal ganglion cells (RGCs). Multiple processes have been proposed to contribute to and/or mediate axonal injury in glaucoma, including: neuroinflammation, loss of neurotrophic factors, dysregulation of the neurovascular unit, and disruption of the axonal cytoskeleton. While the inciting injury to RGCs in glaucoma is complex and potentially heterogeneous, axonal injury is ultimately thought to be the key insult that drives glaucomatous neurodegeneration. Glaucomatous neurodegeneration is a complex process, with multiple molecular signals contributing to RGC somal loss and axonal degeneration. Furthermore, the propagation of the axonal injury signal is complex, with injury triggering programs of degeneration in both the somal and axonal compartment. Further complicating this process is the involvement of multiple cell types that are known to participate in the process of axonal and neuronal degeneration after glaucomatous injury. Here, we review the axonal signaling that occurs after injury and the molecular signaling programs currently known to be important for somal and axonal degeneration after glaucoma-relevant axonal injuries.

Indexed as

AnimalsAxonsGlaucomaHumansIntraocular PressureOptic Nerve InjuriesRetinal Ganglion CellsSignal TransductionApoptosisAxonAxonopathyDendritic remodelingIntraocular pressureNeuroprotectionOptic neuropathySynaptic loss

Identifiers

PMID31301400
PMCPMC6898776
OpenAlexW2960352676

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.