Evidence map›Paper›PMID 24283717›Full record

ArticleBritish journal of pharmacology2014

Deletion of thioredoxin-interacting protein preserves retinal neuronal function by preventing inflammation and vascular injury.

M F El-Azab, B R B Baldowski, B A Mysona, A Y Shanab, I N Mohamed, M A Abdelsaid, S Matragoon, K E Bollinger, A Saul, A B El-Remessy

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Review
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  10. Identification of Effective and Nonpromiscuous Antidiabetic Drug Molecules fromEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
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  14. NOD-like Receptors in the Eye: Uncovering Its Role in Diabetic Retinopathy.International journal of molecular sciences · 2020
    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

10 authors at 4 institutions in 1 country.

M F El-AzabCenter for Pharmacy and Experimental Therapeutics, University of Georgia, Augusta, GA, USA; James and Jean Culver Vision Discovery Institute, Georgia Regents University, Augusta, GA, USA; Charlie Norwood Veterans Affairs Medical Center, Augusta, GA, USA.
B R B Baldowski
B A Mysona
A Y Shanab
I N Mohamed
M A Abdelsaid
S Matragoon
K E Bollinger
A Saul
A B El-Remessy
Discovery Institute · USAugusta University · USUniversity of Georgia · USCharlie Norwood VA Medical Center · US

Funding

Molecular Mechanisms of diabetic retinopathyR01EY022408 · NEI · UNIVERSITY OF GEORGIA · PI EL-REMESSY, AZZA B · 2012 to 2016
$1.5M
NEI NIH HHS EY-022408NEI NIH HHS R01 EY022408
6 · The paper itself

Abstract

background and purposeRetinal neurodegeneration is an early and critical event in several diseases associated with blindness. Clinically, therapies that target neurodegeneration fail. We aimed to elucidate the multiple roles by which thioredoxin-interacting protein (TXNIP) contributes to initial and sustained retinal neurodegeneration. EXPERIMENTAL APPROACH: Neurotoxicity was induced by intravitreal injection of NMDA into wild-type (WT) and TXNIP-knockout (TKO) mice. The expression of apoptotic and inflammatory markers was assessed by immunohistochemistry, elisa and Western blot. Microvascular degeneration was assessed by periodic acid-Schiff and haematoxylin staining and retinal function by electroretinogram. KEY

resultsNMDA induced early (1 day) and significant retinal PARP activation, a threefold increase in TUNEL-positive nuclei and 40% neuronal loss in ganglion cell layer (GCL); and vascular permeability in WT but not TKO mice. NMDA induced glial activation, expression of TNF-α and IL-1β that co-localized with Müller cells in WT but not TKO mice. In parallel, NMDA triggered the expression of NOD-like receptor protein (NLRP3), activation of caspase-1, and release of IL-1β and TNF-α in primary WT but not TKO Müller cultures. After 14 days, NMDA induced 1.9-fold microvascular degeneration, 60% neuronal loss in GCL and increased TUNEL-labelled cells in the GCL and inner nuclear layer in WT but not TKO mice. Electroretinogram analysis showed more significant reductions in b-wave amplitudes in WT than in TKO mice. CONCLUSION AND IMPLICATIONS: Targeting TXNIP expression prevented early retinal ganglion cell death, glial activation, retinal inflammation and secondary neuro/microvascular degeneration and preserved retinal function. TXNIP is a promising new therapeutic target for retinal neurodegenerative diseases.

Indexed as

AdultAgedAnimalsApoptosisCarrier ProteinsCells, CulturedEpendymoglial CellsFemaleGlaucoma, Open-AngleHumansInflammationInterleukin-1betaMaleMiceMice, Inbred C57BLMice, Knockout3-nitrotyrosineCarrier ProteinsInterleukin-1betaN-MethylaspartateThioredoxin-Disulfide ReductaseThioredoxinsTumor Necrosis Factor-alphaTxnip protein, mouseTyrosineacellular capillaryapoptosisERGIL-1βMüller cellneurotoxicityNMDAretinaTNF-αTXNIPvascular permeability

Identifiers

PMID24283717
PMCPMC3952806
OpenAlexW1545890430

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.