Evidence map›Paper›PMID 31211954›Full record

ArticleExperimental eye research2019

Effect of ocular hypertension on the pattern of retinal ganglion cell subtype loss in a mouse model of early-onset glaucoma.

S Daniel, K J Meyer, A F Clark, M G Anderson, C M McDowell

Open access · greenAbstract read
In one paragraph

Article in Experimental eye research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 27 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. DAMPs Drive Fibroinflammatory Changes in the Glaucomatous ONH.Investigative ophthalmology & visual science · 2024
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Differential susceptibility of retinal ganglion cell subtypes against neurodegenerative diseases.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022
    Review
  13. Article
  14. Early-Onset Glaucoma inBiomedicines · 2022
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Non-Cell Autonomous Roles for CASK in Optic Nerve Hypoplasia.Investigative ophthalmology & visual science · 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

5 authors at 3 institutions in 1 country.

S DanielNorth Texas Eye Research Institute, Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, TX, United States.
K J MeyerDepartment of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, United States.
A F ClarkNorth Texas Eye Research Institute, Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, TX, United States.
M G AndersonDepartment of Molecular Physiology and Biophysics, University of Iowa, Iowa City, IA, United States; Department of Ophthalmology and Visual Sciences, University of Iowa, Iowa City, IA, United States; (d)VA Center for the Prevention and Treatment of Visual Loss, Iowa City VA Health Care System, Iowa City, IA, United States.
C M McDowellDepartment of Ophthalmology and Visual Sciences, McPherson Eye Research Institute, University of Wisconsin-Madison, Madison, WI, United States. Electronic address: cmmcdowell@wisc.edu.
University of Iowa · USUniversity of North Texas · USSmith-Kettlewell Eye Research Institute · US

Funding

Stem Cell and Organoid CoreP30EY025580 · NEI · UNIVERSITY OF IOWA · PI TODD E SCHEETZ · 2016 to 2026
$6.9M
Crosstalk Between Unfolded Protein Response and Autophagy for the Treatment of GlaucomaR01EY026177 · NEI · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI ZODE, GULAB · 2016 to 2025
$3.8M
Cross-talk of TGFβ2 and TLR4 in the trabecular meshworkR01EY026529 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI MCDOWELL, COLLEEN MARY · 2016 to 2022
$2.7M
Novel Genome Editing for the Treatment of GlaucomaR01EY030366 · NEI · UNIVERSITY OF IOWA · PI CLARK, ABBOT FREDERICK, SHEFFIELD, VAL C. · 2019 to 2023
$2.7M
Genetic modifiers of Cep290-mediated retinal degenerationR21EY029609 · NEI · UNIVERSITY OF IOWA · PI ANDERSON, MICHAEL G · 2018 to 2019
$419k
Therapy of Nocturnal Intraocular Pressure Elevation Causing Glaucoma ProgressionI01RX001481 · VA · IOWA CITY VA MEDICAL CENTER · PI ANDERSON, MICHAEL G · 2015 to 2019
–
NEI NIH HHS P30 EY025580NEI NIH HHS R01 EY026177NEI NIH HHS R01 EY030366NEI NIH HHS R21 EY029609RRD VA I01 RX001481
6 · The paper itself

Abstract

Glaucoma is a neurodegenerative disease with elevated intraocular pressure as one of the major risk factors. Glaucoma leads to irreversible loss of vision and its progression involves optic nerve head cupping, axonal degeneration, retinal ganglion cell (RGC) loss, and visual field defects. Despite its high global prevalence, glaucoma still remains a major neurodegenerative disease. Introduction of mouse models of experimental glaucoma has become integral to glaucoma research due to well-studied genetics as well as ease of manipulations. Many established inherent and inducible mouse models of glaucoma are used to study the molecular and physiological progression of the disease. One such model of spontaneous mutation is the nee model, which is caused by mutation of the Sh3pxd2b gene. In both humans and mice, mutations disrupting function of the SH3PXD2B adaptor protein cause a developmental syndrome including secondary congenital glaucoma. The purpose of this study was to characterize the early onset nee glaucoma phenotype on the C57BL/6J background and to evaluate the pattern of RGC loss and axonal degeneration in specific RGC subtypes. We found that the B6.Sh3pxd2b

Indexed as

Disease Models, AnimalAnimalsAxonsCell CountCell SurvivalFemaleGlaucomaIntraocular PressureMaleMiceMice, Inbred C57BLOcular HypertensionOptic NervePhenotypePhospholipid Transfer ProteinsRetinal Ganglion CellsFad49 protein, mousePhospholipid Transfer ProteinsGlaucomaIntraocular pressureOptic nerveRGC subtype

Identifiers

PMID31211954
PMCPMC7430001
OpenAlexW2950051250

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.