Evidence map›Paper›PMID 28708137›Full record

ArticleCell death and differentiation2017

FAS apoptotic inhibitory molecule 2 is a stress-induced intrinsic neuroprotective factor in the retina.

Mercy Pawar, Boris Busov, Aaruran Chandrasekhar, Jingyu Yao, David N Zacks, Cagri G Besirli

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 31% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
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  10. Cell Death in AMD: The Rationale for Targeting Fas.Journal of clinical medicine · 2022
    Review
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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

6 authors at 1 institution in 1 country.

Mercy PawarDepartment of Ophthalmology and Visual Sciences, W.K. Kellogg Eye Center, University of Michigan, Ann Arbor, MI 48105, USA.
Boris BusovDepartment of Ophthalmology and Visual Sciences, W.K. Kellogg Eye Center, University of Michigan, Ann Arbor, MI 48105, USA.
Aaruran ChandrasekharDepartment of Ophthalmology and Visual Sciences, W.K. Kellogg Eye Center, University of Michigan, Ann Arbor, MI 48105, USA.
Jingyu YaoDepartment of Ophthalmology and Visual Sciences, W.K. Kellogg Eye Center, University of Michigan, Ann Arbor, MI 48105, USA.
David N ZacksDepartment of Ophthalmology and Visual Sciences, W.K. Kellogg Eye Center, University of Michigan, Ann Arbor, MI 48105, USA.
Cagri G BesirliDepartment of Ophthalmology and Visual Sciences, W.K. Kellogg Eye Center, University of Michigan, Ann Arbor, MI 48105, USA.
University of Michigan–Ann Arbor · US

Funding

VIVARIUM MODULEP30EY007003 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI David Antonetti · 1987 to 2026
$17.6M
Neuroprotection in pediatric retinal detachmentK08EY023982 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BESIRLI, CAGRI · 2014 to 2018
$925k
E75 IN THE DEVELOPING DROSOPHILA EYEF31EY007003 · NEI · YALE UNIVERSITY · PI SHILTON, ALYCIA N · 1999 to 2001
$14k
NEI NIH HHS F31 EY007003NEI NIH HHS K08 EY023982NEI NIH HHS P30 EY007003
6 · The paper itself

Abstract

We report the neuroprotective role of FAS apoptotic inhibitory molecule 2 (FAIM2), an inhibitor of the FAS signaling pathway, during stress-induced photoreceptor apoptosis. Retinal detachment resulted in increased FAIM2 levels in photoreceptors with higher amounts detected at the tips of outer segments. Activation of FAS death receptor via FAS-ligand led to JNK-mediated FAIM2 phosphorylation, decreased proteasome-mediated degradation and increased association with the FAS receptor. Photoreceptor apoptosis was accelerated in Faim2 knockout mice following experimental retinal detachment. We show that FAIM2 is primarily involved in reducing stress-induced photoreceptor cell death but this effect was transient. FAIM2 was found to interact with both p53 and HSP90 following the activation of the FAS death pathway and FAIM2/HSP90 interaction was dependent on the phosphorylation of FAIM2. Lack of FAIM2 led to increased expression of proadeath genes Fas and Ripk1 in the retina under physiologic conditions. These results demonstrate that FAIM2 is an intrinsic neuroprotective factor activated by stress in photoreceptors and delays FAS-mediated photoreceptor apoptosis. Modulation of this pathway to increase FAIM2 expression may be a potential therapeutic option to prevent photoreceptor death.

Indexed as

AnimalsApoptosisCell DeathFas Ligand Proteinfas ReceptorIntrinsic FactorMembrane ProteinsMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsPhotoreceptor CellsRetinaFas Ligand Proteinfas ReceptorIntrinsic Factorlifeguard protein, mouseMembrane ProteinsNerve Tissue Proteins

Identifiers

PMID28708137
PMCPMC5596422
OpenAlexW2735220895

What OpenQuestion holds

Textmetadata
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.