Evidence map›Paper›PMID 31122676›Full record

ArticleNeuron2019

Elevating Growth Factor Responsiveness and Axon Regeneration by Modulating Presynaptic Inputs.

Yiling Zhang, Philip R Williams, Anne Jacobi, Chen Wang, Anurag Goel, Arlene A Hirano, Nicholas C Brecha, Daniel Kerschensteiner, Zhigang He

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

80 citing papers in PubMed, 136 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Non-synaptic Mechanism of Ocular Dominance Plasticity.bioRxiv : the preprint server for biology · 2025
    Article
  13. The Role of Methylation Modification in Neural Injury and Repair.International journal of molecular sciences · 2025
    Review
  14. Roles of Kdm6a and Kdm6b in Regulation of Mammalian Neural Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review

20 more citing papers are in PubMed but not listed here.

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

9 authors at 4 institutions in 1 country.

Yiling ZhangF.M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, Boston, MA, USA.
Philip R WilliamsF.M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, Boston, MA, USA; Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, MO, USA. Electronic address: prwillia@wustl.edu.
Anne JacobiF.M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, Boston, MA, USA.
Chen WangF.M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, Boston, MA, USA.
Anurag GoelDepartment of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, MO, USA.
Arlene A HiranoDepartment of Neurobiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; United States Veterans Administration Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
Nicholas C BrechaDepartment of Neurobiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; United States Veterans Administration Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
Daniel KerschensteinerDepartment of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, MO, USA.
Zhigang HeF.M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, Boston, MA, USA.
Boston Children's Hospital · USHarvard University · USUniversity of California, Los Angeles · USVA Greater Los Angeles Healthcare System · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
Viral ModuleP30EY012196 · NEI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI ZHIGANG HE · 1998 to 2026
$21.3M
Transmitter Release From Mammalian Horizontal Cells.R01EY015573 · NEI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BRECHA, NICHOLAS C. · 2005 to 2017
$4.9M
SYNAPTIC ORGANIZATION AND VISUAL PROCESSING IN INTERNEURON CIRCUITS OF THE RETINAR01EY026978 · NEI · WASHINGTON UNIVERSITY · PI Daniel Kerschensteiner · 2016 to 2026
$3.8M
Synapse rescue and neuroprotection in the retinaR01EY027411 · NEI · WASHINGTON UNIVERSITY · PI Daniel Kerschensteiner · 2017 to 2026
$3.4M
Neuronal plasticity in retinal circuit development and diseaseR01EY023341 · NEI · WASHINGTON UNIVERSITY · PI KERSCHENSTEINER, DANIEL · 2014 to 2022
$2.8M
Horizontal cell signaling in the mammalian retinaR01EY029869 · NEI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BRECHA, NICHOLAS C. · 2019 to 2023
$2.8M
BLRD VA I01 BX000764BLRD VA IK6 BX005230NEI NIH HHS P30 EY012196NEI NIH HHS R01 EY015573NEI NIH HHS R01 EY023341NEI NIH HHS R01 EY026978NEI NIH HHS R01 EY027411NEI NIH HHS R01 EY029869NICHD NIH HHS P30 HD018655
6 · The paper itself

Abstract

Despite robust effects on immature neurons, growth factors minimally promote axon regeneration in the adult central nervous system (CNS). Attempting to improve growth-factor responsiveness in mature neurons by dedifferentiation, we overexpressed Lin28 in the retina. Lin28-treated retinas responded to insulin-like growth factor-1 (IGF1) by initiating retinal ganglion cell (RGC) axon regeneration after axotomy. Surprisingly, this effect was cell non-autonomous. Lin28 expression was required only in amacrine cells, inhibitory neurons that innervate RGCs. Ultimately, we found that optic-nerve crush pathologically upregulated activity in amacrine cells, which reduced RGC electrical activity and suppressed growth-factor signaling. Silencing amacrine cells or pharmacologically blocking inhibitory neurotransmission also induced IGF1 competence. Remarkably, RGCs regenerating across these manipulations localized IGF1 receptor to their primary cilia, which maintained their signaling competence and regenerative ability. Thus, our results reveal a circuit-based mechanism that regulates CNS axon regeneration and implicate primary cilia as a regenerative signaling hub.

Indexed as

Amacrine CellsAnimalsAxonsCiliaInsulin-Like Growth Factor IMiceMice, Inbred C57BLNerve CrushNerve Growth FactorNerve RegenerationOptic Nerve InjuriesReceptor, IGF Type 1Receptors, PresynapticRetinaRetinal Ganglion CellsRNA-Binding ProteinsInsulin-Like Growth Factor ILin-28 protein, mouseNerve Growth FactorReceptor, IGF Type 1Receptors, PresynapticRNA-Binding Proteins

Identifiers

PMID31122676
PMCPMC7350660
OpenAlexW2946658992

What OpenQuestion holds

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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.