Evidence map›Paper›PMID 25086184›Full record

ArticleMicrovascular research2014

IGFBP-3 inhibits TNF-α production and TNFR-2 signaling to protect against retinal endothelial cell apoptosis.

Qiuhua Zhang, Jena J Steinle

Abstract read
In one paragraph

Article in Microvascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.4field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

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  12. PKA regulates HMGB1 through activation of IGFBP-3 and SIRT1 in human retinal endothelial cells cultured in high glucose.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Article
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  16. Review
  17. Protective effects of agonists of growth hormone-releasing hormone (GHRH) in early experimental diabetic retinopathy.Proceedings of the National Academy of Sciences of the United States of America · 2017
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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

2 authors at 1 institution in 1 country.

Qiuhua ZhangDepartment of Ophthalmology, University of Tennessee Health Science Center, Memphis, TN, USA.
Jena J SteinleDepartment of Ophthalmology, University of Tennessee Health Science Center, Memphis, TN, USA; Department of Anatomy & Neurobiology, University of Tennessee Health Science Center, Memphis, TN, USA; Department of Pharmaceutical Sciences, University of Tennessee Health Science Center, Memphis, TN, USA. Electronic address: jsteinl1@uthsc.edu.
University of Tennessee Health Science Center · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
CORE--MOLECULAR BIOLOGYP30EY013080 · NEI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI JOHNSON, DIANNA AMMONS · 2000 to 2010
$3.7M
Compound 49b Prevents Retinal Endothelial Cell Death Through IGFBP-3 LevelsR01EY022045 · NEI · WAYNE STATE UNIVERSITY · PI STEINLE, JENA J · 2012 to 2016
$1.8M
NEI NIH HHS 3P30 EY013080NEI NIH HHS P30 EY013080NEI NIH HHS R01 EY022045NEI NIH HHS R01EY022045NIDDK NIH HHS P30 DK020572
6 · The paper itself

Abstract

In models of diabetic retinopathy, insulin-like growth factor binding protein-3 (IGFBP-3) protects against tumor necrosis factors-alpha (TNF-α)-mediated apoptosis of retinal microvascular endothelial cells (REC), but the underlying mechanisms are unclear. Our current findings suggest that at least two discrete but complimentary pathways contribute to the protective effects of IGFBP-3; 1) IGFBP-3 directly activates the c-Jun kinase/tissue inhibitor of metalloproteinase-3/TNF-α converting enzyme (c-Jun/TIMP-3/TACE), pathway, which in turn inhibits TNF-α production; 2) IGFBP-3 acts through the IGFBP-3 receptor, low-density lipoprotein receptor-related protein 1 (LRP1), to inhibit signaling of TNF-α receptor 2 (TNFR2). Combined, these two IGFBP-3 pathways substantially reduce REC apoptosis and offer potential targets for the treatment of diabetic retinopathy.

Indexed as

ApoptosisSignal TransductionADAM17 ProteinADAM ProteinsCells, CulturedDiabetic RetinopathyEndothelial CellsHumansInsulin-Like Growth Factor Binding Protein 3JNK Mitogen-Activated Protein KinasesLow Density Lipoprotein Receptor-Related Protein-1Receptors, Tumor Necrosis Factor, Type IIRetinal VesselsTissue Inhibitor of Metalloproteinase-3TransfectionTumor Necrosis Factor-alphaADAM17 ProteinADAM17 protein, humanADAM ProteinsIGFBP3 protein, humanInsulin-Like Growth Factor Binding Protein 3JNK Mitogen-Activated Protein KinasesLow Density Lipoprotein Receptor-Related Protein-1LRP1 protein, humanReceptors, Tumor Necrosis Factor, Type IITIMP3 protein, humanTissue Inhibitor of Metalloproteinase-3TNFRSF1B protein, humanTumor Necrosis Factor-alphaApoptosisc-JunDiabetic retinopathyIGFBP-3TNFalpha

Identifiers

PMID25086184
PMCPMC4346193
OpenAlexW1970794158

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.