Evidence map›Paper›PMID 32165410›Full record

ArticleeNeuro

Targeted Krüppel-Like Factor 4 Gene Knock-Out in Retinal Ganglion Cells Improves Visual Function in Multiple Sclerosis Mouse Model.

Venu Talla, Rajeshwari Koilkonda

Open access · goldAbstract read
In one paragraph

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 47% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
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.

Venu TallaBascom Palmer Eye Institute, Department of Ophthalmology, University of Miami, Miller School of Medicine, Miami, FL 33136 vtalla@miami.edu.ORCID 0000-0002-5695-7536
Rajeshwari KoilkondaBascom Palmer Eye Institute, Department of Ophthalmology, University of Miami, Miller School of Medicine, Miami, FL 33136.
University of Miami · US

Funding

Shared Equipment ModuleP30EY014801 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Dmitry V Ivanov · 2004 to 2026
$12.2M
NEI NIH HHS P30 EY014801
6 · The paper itself

Abstract

Axonal demyelination injury and neuronal degeneration are the primary causes of visual disability in multiple sclerosis (MS)-linked optic neuritis patients. Immunomodulatory therapies targeting inflammation have failed to avert the disease progression and no therapies exist to prevent the neuronal deficits seen in MS to date. Neuroprotective strategies targeting oligodendrocytes and astroglia have shown limited success due to a lack of axonal regeneration from injured neurons. In this study, we used the chronic experimental autoimmune encephalomyelitis (EAE) mouse model of MS to investigate the axonal regenerative approach to improve the neuronal function. Our approach focused on targeted knock-out (KO) of the developmentally regulated axon growth inhibitory Krüppel-like factor 4 (

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalMultiple SclerosisOptic NeuritisAnimalsDisease Models, AnimalHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMiceMice, Inbred C57BLRetinal Ganglion CellsKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription Factorsaxon regenerationdemyelinationEAEMSneuroprotectionoptic neuritis

Identifiers

PMID32165410
PMCPMC7139550
OpenAlexW3011103373

What OpenQuestion holds

Textmetadata
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.