Evidence map›Paper›PMID 31273087›Full record

ArticleDevelopment (Cambridge, England)2019

Human retinal ganglion cell axon regeneration by recapitulating developmental mechanisms: effects of recruitment of the mTOR pathway.

Pooja Teotia, Matthew J Van Hook, Dietmar Fischer, Iqbal Ahmad

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.8field-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

38 citing papers in PubMed, 46 citations in OpenAlex.

  1. Neuroinflammation in glaucoma: a myriad of cellular pathways and players.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  2. Article
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  4. [Retinal protective effects of zincZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Article
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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

4 authors at 2 institutions in 2 countries.

Pooja TeotiaDepartment of Ophthalmology and Visual Science, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Matthew J Van HookDepartment of Ophthalmology and Visual Science, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Dietmar FischerDepartment of Cell Physiology, Ruhr University of Bochum, Universitätsstraße 150, 44780 Bochum, Germany.
Iqbal AhmadDepartment of Ophthalmology and Visual Science, University of Nebraska Medical Center, Omaha, NE 68198, USA iahmad@unmc.edu.ORCID 0000-0003-1920-9835
University of Nebraska Medical Center · USHeinrich Heine University Düsseldorf · DE

Funding

Induced pluripotent stem cell approach to optic nerve regenerationR01EY022051 · NEI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI AHMAD, IQBAL · 2013 to 2022
$3.4M
Human Disease Modeling of Glaucomatous NeuropathyR01EY029778 · NEI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI AHMAD, IQBAL · 2019 to 2022
$1.7M
NEI NIH HHS R01 EY022051NEI NIH HHS R01 EY029778
6 · The paper itself

Abstract

The poor axon regeneration in the central nervous system (CNS) often leads to permanent functional deficit following disease or injury. For example, degeneration of retinal ganglion cell (RGC) axons in glaucoma leads to irreversible loss of vision. Here, we have tested the hypothesis that the mTOR pathway regulates the development of human RGCs and that its recruitment after injury facilitates axon regeneration. We observed that the mTOR pathway is active during RGC differentiation, and using the induced pluripotent stem cell model of neurogenesis show that it facilitates the differentiation, function and neuritogenesis of human RGCs. Using a microfluidic model, we demonstrate that recruitment of the mTOR pathway facilitates human RGC axon regeneration after axotomy, providing evidence that the recapitulation of developmental mechanism(s) might be a viable approach for facilitating axon regeneration in the diseased or injured human CNS, thus helping to reduce and/or recover loss of function.

Indexed as

Nerve RegenerationAdultAnimalsAxonsCell DifferentiationCells, CulturedEmbryo, MammalianEmbryonic DevelopmentFemaleGene Expression Regulation, DevelopmentalHumansPregnancyRatsRats, Sprague-DawleyRetinal Ganglion CellsSignal TransductionMTOR protein, humanTOR Serine-Threonine KinasesDevelopmentGlaucomamTORRegenerationRetinaRGC

Identifiers

PMID31273087
PMCPMC6633601
OpenAlexW2954710602

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.