Evidence map›Paper›PMID 16103918›Full record

ArticlePLoS genetics2005

Susceptibility to neurodegeneration in a glaucoma is modified by Bax gene dosage.

Richard T Libby, Yan Li, Olga V Savinova, Joseph Barter, Richard S Smith, Robert W Nickells, Simon W M John

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
229citing papers in PubMed, 1 pooled it
14.5field-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

229 citing papers in PubMed, 1 synthesis or guideline pooled it, 364 citations in OpenAlex.

  1. Pooled it
  2. Peripheral Neuropathy in Metabolic Stress.International journal of molecular sciences · 2026
    Review
  3. Neuroinflammation in glaucoma: a myriad of cellular pathways and players.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Axonal mitophagy in retinal ganglion cells.Cell communication and signaling : CCS · 2024
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

169 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

7 authors at 4 institutions in 1 country.

Richard T LibbyThe Jackson Laboratory, Bar Harbor, Maine, USA.
Yan Li
Olga V Savinova
Joseph Barter
Richard S Smith
Robert W Nickells
Simon W M John
Jackson Laboratory · USHoward Hughes Medical Institute · USTufts University · USUniversity of Wisconsin–Madison · US

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI Anna Karolina Palucka · 1985 to 2026
$61.9M
MOLECULAR MECHANISM OF RETINAL GANGLION CELL DEATHR29EY012223 · NEI · UNIVERSITY OF WISCONSIN MADISON · PI NICKELLS, ROBERT W · 1998 to 2002
$310k
Testing therapeutic pathways in genetic glaucomaF32EY014515 · NEI · JACKSON LABORATORY · PI LIBBY, RICHARD T · 2003 to 2004
$106k
NCI NIH HHS P30 CA034196NEI NIH HHS F32 EY014515NEI NIH HHS R29 EY012223
6 · The paper itself

Abstract

In glaucoma, harmful intraocular pressure often contributes to retinal ganglion cell death. It is not clear, however, if intraocular pressure directly insults the retinal ganglion cell axon, the soma, or both. The pathways that mediate pressure-induced retinal ganglion cell death are poorly defined, and no molecules are known to be required. DBA/2J mice deficient in the proapoptotic molecule BCL2-associated X protein (BAX) were used to investigate the roles of BAX-mediated cell death pathways in glaucoma. Both Bax+/- and Bax-/- mice were protected from retinal ganglion cell death. In contrast, axonal degeneration was not prevented in either Bax+/- or Bax-/- mice. While BAX deficiency did not prevent axonal degeneration, it did slow axonal loss. Additionally, we compared the effects of BAX deficiency on the glaucoma to its effects on retinal ganglion cell death due to two insults that are proposed to participate in glaucoma. As in the glaucoma, BAX deficiency protected retinal ganglion cells after axon injury by optic nerve crush. However, it did not protect retinal ganglion cells from N-methyl-D-aspartate (NMDA)-induced excitotoxicity. BAX is required for retinal ganglion cell death in an inherited glaucoma; however, it is not required for retinal ganglion cell axon degeneration. This indicates that distinct somal and axonal degeneration pathways are active in this glaucoma. Finally, our data support a role for optic nerve injury but not for NMDA receptor-mediated excitotoxicity in this glaucoma. These findings indicate a need to understand axon-specific degeneration pathways in glaucoma, and they suggest that distinct somal and axonal degeneration pathways may need to be targeted to save vision.

Identifiers

PMID16103918
PMCPMC1183523
OpenAlexW2055335620

What OpenQuestion holds

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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.