Evidence map›Paper›PMID 31839616›Full record

ReviewRestorative neurology and neuroscience2019

Lab review: Molecular dissection of the signal transduction pathways associated with PTEN deletion-induced optic nerve regeneration.

Haoliang Huang, Simran Kaur, Yang Hu

Open access · greenAbstract readReview
In one paragraph

Review in Restorative neurology and neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 37% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. 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

3 authors at 1 institution in 1 country.

Haoliang HuangDepartment of Ophthalmology, Stanford University School of Medicine, Palo Alto, CA, USA.
Simran KaurDepartment of Ophthalmology, Stanford University School of Medicine, Palo Alto, CA, USA.
Yang HuDepartment of Ophthalmology, Stanford University School of Medicine, Palo Alto, CA, USA.
Stanford University · US

Funding

Stanford Vision Research CoreP30EY026877 · NEI · STANFORD UNIVERSITY · PI Jeffrey L Goldberg · 2017 to 2026
$8.0M
Elucidating Neuron-Intrinsic Molecular Mechanisms of Optic Nerve RegenerationR01EY024932 · NEI · TEMPLE UNIV OF THE COMMONWEALTH · PI Yang Hu · 2015 to 2026
$4.8M
Neuroprotection by Modulating ER Stress in GlaucomaR01EY023295 · NEI · TEMPLE UNIV OF THE COMMONWEALTH · PI HU, YANG · 2013 to 2022
$3.8M
Developing Novel Neuroprotective Strategies for EAE/Optic NeuritisR01EY028106 · NEI · STANFORD UNIVERSITY · PI HU, YANG · 2018 to 2021
$1.9M
NEI NIH HHS P30 EY026877NEI NIH HHS R01 EY023295NEI NIH HHS R01 EY024932NEI NIH HHS R01 EY028106
6 · The paper itself

Abstract

backgroundPermanent loss of vital functions after central nervous system (CNS) injury occurs in part because axons in the adult mammalian CNS do not regenerate after injury. PTEN was identified as a prominent intrinsic inhibitor of CNS axon regeneration about 10 years ago. The PTEN negatively regulated PI3K-AKT-mTOR pathway, which has been intensively explored in diverse models of axon injury and diseases and its mechanism for axon regeneration is becoming clearer.

objectiveIt is timely to summarize current knowledge about the PTEN/AKT/mTOR pathway and discuss future directions of translational regenerative research for neural injury and neurodegenerative diseases.

methodsUsing mouse optic nerve crush as an in vivo retinal ganglion cell axon injury model, we have conducted an extensive molecular dissection of the PI3K-AKT-mTORC1/mTORC2 pathway to illuminate the cross-regulating mechanisms in axon regeneration.

resultsAKT is the nodal point that coordinates both positive (PI3K-PDK1-pAKT-T308) and negative (PI3K-mTORC2-pAKT-S473) signals to regulate adult CNS axon regeneration through two parallel pathways, activating mTORC1 and inhibiting GSK3β. However, mTORC1/S6K1-mediated feedback inhibition after PTEN deletion prevents potent AKT activation.

conclusionsA key permissive signal from an unidentified AKT-independent pathway is required for stimulating the neuron-intrinsic growth machinery. Future studies into this complex neuron-intrinsic balancing mechanism involving necessary and permissive signals for axon regeneration is likely to lead to safe and effective regenerative strategies for CNS repair.

Indexed as

AnimalsMiceNerve RegenerationOptic NerveOptic Nerve InjuriesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionTOR Serine-Threonine KinasesmTOR protein, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouseTOR Serine-Threonine KinasesAKTAxon regenerationmTOROptic NervePTENRGC

Identifiers

PMID31839616
PMCPMC6938454
OpenAlexW2996169568

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.