Evidence map›Paper›PMID 23894672›Full record

ArticlePloS one2013

β2-adrenergic receptor knockout mice exhibit A diabetic retinopathy phenotype.

Youde Jiang, Qiuhua Zhang, Li Liu, Jie Tang, Timothy S Kern, Jena J Steinle

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  7. TLR4 regulates insulin-resistant proteins to increase apoptosis in the mouse retina.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
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  12. Adrenergic and serotonin receptors affect retinal superoxide generation in diabetic mice: relationship to capillary degeneration and permeability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
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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 3 institutions in 1 country.

Youde JiangDepartment of Ophthalmology, University of Tennessee Health Science Center, Memphis, Tennessee, United States of America.
Qiuhua Zhang
Li Liu
Jie Tang
Timothy S Kern
Jena J Steinle
University of Tennessee Health Science Center · USCase Western Reserve University · USLouis Stokes Cleveland VA Medical Center · US

Funding

STUDY OF DIABETIC RETINOPATHYR01EY000300 · NEI · UNIVERSITY OF WISCONSIN MADISON · PI KERN, TIMOTHY S · 1985 to 2013
$4.7M
CORE--MOLECULAR BIOLOGYP30EY013080 · NEI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI JOHNSON, DIANNA AMMONS · 2000 to 2010
$3.7M
Vision Research CoreP30EY021721 · NEI · UNIVERSITY OF FLORIDA · PI HAUSWIRTH, WILLIAM W · 2011 to 2015
$2.8M
Compound 49b Prevents Retinal Endothelial Cell Death Through IGFBP-3 LevelsR01EY022045 · NEI · WAYNE STATE UNIVERSITY · PI STEINLE, JENA J · 2012 to 2016
$1.8M
Study of diabetic retinopathyR56EY000300 · NEI · CASE WESTERN RESERVE UNIVERSITY · PI KERN, TIMOTHY S · 2009 to 2009
$353k
NEI NIH HHS EY00300NEI NIH HHS EY013080NEI NIH HHS P30 EY013080NEI NIH HHS P30 EY021721NEI NIH HHS R01 EY000300NEI NIH HHS R01 EY022045NEI NIH HHS R01EY022045NEI NIH HHS R56 EY000300PHS HHS 2-2011-597
6 · The paper itself

Abstract

There is considerable evidence from our lab and others for a functional link between β-adrenergic receptor and insulin receptor signaling pathways in retina. Furthermore, we hypothesize that this link may contribute to lesions similar to diabetic retinopathy in that the loss of adrenergic input observed in diabetic retinopathy may disrupt normal anti-apoptotic insulin signaling, leading to retinal cell death. Our studies included assessment of neural retina function (ERG), vascular degeneration, and Müller glial cells (which express only β1 and β2-adrenergic receptor subtypes). In the current study, we produced β2-adrenergic receptor knockout mice to examine this deletion on retinal neurons and vasculature, and to identify specific pathways through which β2-adrenergic receptor modulates insulin signaling. As predicted from our hypothesis, β2-adrenergic receptor knockout mice display certain features similar to diabetic retinopathy. In addition, loss of β2-adrenergic input resulted in an increase in TNFα, a key inhibitor of insulin receptor signaling. Increased TNFα may be associated with insulin-dependent production of the anti-apoptotic factor, Akt. Since the effects occurred in vivo under normal glucose conditions, we postulate that aspects of the diabetic retinopathy phenotype might be triggered by loss of β2-adrenergic receptor signaling.

Indexed as

AnimalsBlotting, WesternDiabetic RetinopathyEnzyme-Linked Immunosorbent AssayImmunohistochemistryIn Situ Nick-End LabelingIn Vitro TechniquesMiceMice, KnockoutReceptors, Adrenergic, beta-2Tumor Necrosis Factor-alphaReceptors, Adrenergic, beta-2Tumor Necrosis Factor-alpha

Identifiers

PMID23894672
PMCPMC3722144
OpenAlexW2018887860

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.