Evidence map›Paper›PMID 28064040›Full record

ReviewProgress in retinal and eye research2017

BAX to basics: How the BCL2 gene family controls the death of retinal ganglion cells.

Margaret E Maes, Cassandra L Schlamp, Robert W Nickells

Abstract readReview
In one paragraph

Review in Progress in retinal and eye research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 2% 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

107 citing papers in PubMed, 2 syntheses or guidelines pooled it, 193 citations in OpenAlex.

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  11. 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
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47 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

3 authors at 1 institution in 1 country.

Margaret E MaesDepartment 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
Graduate Training In Cellular And Molecular Pathogenesis Of Human DiseasesT32GM081061 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI FABRY, ZSUZSANNA · 2010 to 2019
$1.8M
Spectral domain optical coherence tomography instrument for multimodal imagingS10OD018221 · OD · UNIVERSITY OF WISCONSIN-MADISON · PI MCLELLAN, GILLIAN JANE · 2014 to 2014
$210k
NEI NIH HHS P30 EY016665NEI NIH HHS R01 EY012223NIGMS NIH HHS T32 GM081061NIH HHS S10 OD018221
6 · The paper itself

Abstract

Retinal ganglion cell (RGC) death is the principal consequence of injury to the optic nerve. For several decades, we have understood that the RGC death process was executed by apoptosis, suggesting that there may be ways to therapeutically intervene in this cell death program and provide a more direct treatment to the cells and tissues affected in diseases like glaucoma. A major part of this endeavor has been to elucidate the molecular biological pathways active in RGCs from the point of axonal injury to the point of irreversible cell death. A major component of this process is the complex interaction of members of the BCL2 gene family. Three distinct family members of proteins orchestrate the most critical junction in the apoptotic program of RGCs, culminating in the activation of pro-apoptotic BAX. Once active, BAX causes irreparable damage to mitochondria, while precipitating downstream events that finish off a dying ganglion cell. This review is divided into two major parts. First, we summarize the extent of knowledge of how BCL2 gene family proteins interact to facilitate the activation and function of BAX. This area of investigation has rapidly changed over the last few years and has yielded a dramatically different mechanistic understanding of how the intrinsic apoptotic program is run in mammalian cells. Second, we provided a comprehensive analysis of nearly two decades of investigation of the role of BAX in the process of RGC death, much of which has provided many important insights into the overall pathophysiology of diseases like glaucoma.

Indexed as

AnimalsApoptosisbcl-2-Associated X ProteinCell DeathGlaucomaHumansOptic NerveOptic Nerve DiseasesProto-Oncogene Proteins c-bcl-2Retinal Ganglion CellsSignal Transductionbcl-2-Associated X ProteinBCL2 protein, humanProto-Oncogene Proteins c-bcl-2BAXBCL2 gene familyBH3-only proteinsGlaucomaIntrinsic and extrinsic apoptosisMitochondrial outer membraneNeuroinflammationRetinal ganglion cellsSecondary degeneration

Identifiers

PMID28064040
PMCPMC5350025
OpenAlexW2568594876

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.