Evidence map›Paper›PMID 29747701›Full record

ArticleActa neuropathologica communications2018

Astrocyte remodeling without gliosis precedes optic nerve Axonopathy.

Melissa L Cooper, John W Collyer, David J Calkins

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Astrocytes in the mouse brain respond bilaterally to unilateral retinal neurodegeneration.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. Article
  8. Glaucomatous retinal ganglion cells: death and protection.International journal of ophthalmology · 2025
    Review
  9. Neuritin 1 Drives Therapeutic Preservation of Retinal Ganglion Cells in anJournal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Astrocyte Immune Functions and Glaucoma.International journal of molecular sciences · 2023
    Review
  16. Aging Effects on Optic Nerve Neurodegeneration.International journal of molecular sciences · 2023
    Review
  17. Astrocyte polarization in glaucoma: a new opportunity.Neural regeneration research · 2022
    Review
  18. Article
  19. Review
  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

3 authors at 1 institution in 1 country.

Melissa L CooperDepartment of Ophthalmology and Visual Sciences, The Vanderbilt Eye Institute, Vanderbilt University Medical Center, 1105 Medical Research Building IV, Nashville, TN, 37232-0654, USA.
John W CollyerDepartment of Ophthalmology and Visual Sciences, The Vanderbilt Eye Institute, Vanderbilt University Medical Center, 1105 Medical Research Building IV, Nashville, TN, 37232-0654, USA.
David J CalkinsDepartment of Ophthalmology and Visual Sciences, The Vanderbilt Eye Institute, Vanderbilt University Medical Center, 1105 Medical Research Building IV, Nashville, TN, 37232-0654, USA. david.j.calkins@vanderbilt.edu.
Vanderbilt University Medical Center · US

Funding

VANDERBILT UNIVERSITY CTSA FOR PEDIATRIC RESEARCHUL1RR024975 · NCRR · VANDERBILT UNIVERSITY · PI BERNARD, GORDON RAPHAEL · 2007 to 2011
$45.7M
Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI David J. Calkins · 1989 to 2026
$19.6M
Training in Vision ResearchT32EY007135 · NEI · VANDERBILT UNIVERSITY · PI GEOFFREY F WOODMAN · 1994 to 2026
$5.8M
Transient Receptor Potential Channels and Retinal Ganglion Cell Death in GlaucomaR01EY017427 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI CALKINS, DAVID J. · 2008 to 2020
$4.2M
Mechanisms of Synaptic Remodeling and Neuronal Self-Repair in Aging and GlaucomaR01EY024997 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI David J. Calkins · 2015 to 2026
$3.8M
NCRR NIH HHS UL1 RR024975NEI NIH HHS EY008126NEI NIH HHS EY024997NEI NIH HHS P30 EY008126NEI NIH HHS R01 EY017427NEI NIH HHS R01 EY024997NEI NIH HHS T32 EY007135Research to Prevent Blindness Senior Investigator AwardSchool of Medicine, Vanderbilt University Stanley Cohen Innovation Fund
6 · The paper itself

Abstract

Astroyctes serve myriad functions but are especially critical in white matter tracts, where energy-demanding axons propagate action potentials great distances between neurons. Axonal dependence on astrocytes for even normal function accentuates the critical role astrocytes serve during disease. In glaucoma, the most common optic neuropathy, sensitivity to intraocular pressure (IOP) challenges RGC axons early, including degradation of anterograde transport to the superior colliculus (SC). Astrocyte remodeling presages overt axon degeneration in glaucoma and thus may present a therapeutic opportunity. Here we developed a novel metric to quantify organization of astrocyte processes in the optic nerve relative to axon degeneration in the DBA/2 J hereditary mouse model of glaucoma. In early progression, as axons expand prior to loss, astrocyte processes become more parallel with migration to the nerve's edge without a change in overall coverage of the nerve. As axons degenerate, astrocyte parallelism diminishes with increased glial coverage and reinvasion of the nerve. In longitudinal sections through aged DBA/2 J nerve, increased astrocyte parallelism reflected elevated levels of the astrocyte gap-junction protein connexin 43 (Cx43). In the distal nerve, increased Cx43 also indicated with a higher level of intact anterograde transport from retina to SC. Our results suggest that progression of axonopathy in the optic nerve involves astrocyte remodeling in two phases. In an early phase, astrocyte processes organize in parallel, likely through gap-junction coupling, while a later phase involves deterioration of organization as glial coverage increases and axons are lost.

Indexed as

AnimalsAstrocytesCholera ToxinDisease Models, AnimalDisease ProgressionEye ProteinsGliosisIntraocular PressureMembrane GlycoproteinsMiceMice, Inbred DBAMice, TransgenicOptic NerveOptic Nerve DiseasesCholera ToxinEye ProteinsGpnmb protein, mouseMembrane GlycoproteinsAstrocytesAxonopathyConnexin 43GlaucomaGliaNeurodegenerationRetinal ganglion cell

Identifiers

PMID29747701
PMCPMC5946396
OpenAlexW2799884241

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.