Evidence map›Paper›PMID 22384122›Full record

ArticlePloS one2012

Genetic ablation of Pannexin1 protects retinal neurons from ischemic injury.

Galina Dvoriantchikova, Dmitry Ivanov, David Barakat, Alexander Grinberg, Rong Wen, Vladlen Z Slepak, Valery I Shestopalov

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

71 citing papers in PubMed, 121 citations in OpenAlex.

  1. Altered Pannexin2 Expression in Retinal Degeneration: Insights from the P23H Mouse Model of Retinis Pigmentosa.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Article
  2. Review
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  4. Mechanobiology in the eye.npj biological physics and mechanics · 2025
    Review
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  19. Pannexin 1 Transgenic Mice: Human Diseases and Sleep-Wake Function Revision.International journal of molecular sciences · 2021
    Article
  20. Article

11 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 2 institutions in 2 countries.

Galina DvoriantchikovaDepartment of Ophthalmology, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, Florida, United States of America.
Dmitry Ivanov
David Barakat
Alexander Grinberg
Rong Wen
Vladlen Z Slepak
Valery I Shestopalov
University of Miami · USNational Institutes of Health · US

Funding

Shared Equipment ModuleP30EY014801 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Victor L Perez · 2004 to 2026
$12.2M
The Role of Pannexin 1 Pathway in Ocular Hypertension Injury of Retinal Ganglion CellsR01EY021517 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SHESTOPALOV, VALERY I · 2012 to 2020
$3.1M
Light-dependent Transducin Movement in Retinal Rods.R01EY018666 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SLEPAK, VLADLEN Z · 2009 to 2013
$1.8M
CNTF and retinal degeneration: the role of Muller cellsR01EY018586 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI WEN, RONG · 2008 to 2011
$1.5M
The role of cell death signals in retinal ischemiaR21EY020613 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI IVANOV, DMITRY V · 2010 to 2011
$406k
The role of NFkB in glia-neuron crosstalk in glaucomaR21EY017991 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SHESTOPALOV, VALERY I · 2007 to 2008
$401k
NEI NIH HHS P30 EY014801NEI NIH HHS R01EY017991NEI NIH HHS R01 EY018586NEI NIH HHS R01EY018586NEI NIH HHS R01 EY018666NEI NIH HHS R01EY018666NEI NIH HHS R01 EY021517NEI NIH HHS R21 EY017991NEI NIH HHS R21 EY020613NEI NIH HHS R21EY020613
6 · The paper itself

Abstract

Pannexin1 (Panx1) forms large nonselective membrane channel that is implicated in paracrine and inflammatory signaling. In vitro experiments suggested that Panx1 could play a key role in ischemic death of hippocampal neurons. Since retinal ganglion cells (RGCs) express high levels of Panx1 and are susceptible to ischemic induced injury, we hypothesized that Panx1 contributes to rapid and selective loss of these neurons in ischemia. To test this hypothesis, we induced experimental retinal ischemia followed by reperfusion in live animals with the Panx1 channel genetically ablated either in the entire mouse (Panx1 KO), or only in neurons using the conditional knockout (Panx1 CKO) technology. Here we report that two distinct neurotoxic processes are induced in RGCs by ischemia in the wild type mice but are inactivated in Panx1KO and Panx1 CKO animals. First, the post-ischemic permeation of RGC plasma membranes is suppressed, as assessed by dye transfer and calcium imaging assays ex vivo and in vitro. Second, the inflammasome-mediated activation of caspase-1 and the production of interleukin-1β in the Panx1 KO retinas are inhibited. Our findings indicate that post-ischemic neurotoxicity in the retina is mediated by previously uncharacterized pathways, which involve neuronal Panx1 and are intrinsic to RGCs. Thus, our work presents the in vivo evidence for neurotoxicity elicited by neuronal Panx1, and identifies this channel as a new therapeutic target in ischemic pathologies.

Indexed as

AllelesAnimalsCalciumConnexinsGlucoseHippocampusInflammationInterleukin-1betaIschemiaMaleMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsOxygenReperfusion InjuryCalciumConnexinsGlucoseInterleukin-1betaNerve Tissue ProteinsOxygenPanx1 protein, mouse

Identifiers

PMID22384122
PMCPMC3285635
OpenAlexW2061512105

What OpenQuestion holds

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Registered trials

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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.