Evidence map›Paper›PMID 25937169›Full record

ArticleNeuron2015

Injury-induced decline of intrinsic regenerative ability revealed by quantitative proteomics.

Stephane Belin, Homaira Nawabi, Chen Wang, Shaojun Tang, Alban Latremoliere, Peter Warren, Hubert Schorle, Ceren Uncu, Clifford J Woolf, Zhigang He and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed, 1 pooled it
10.6field-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

151 citing papers in PubMed, 1 synthesis or guideline pooled it, 258 citations in OpenAlex.

  1. Pooled it
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  13. Roles of Kdm6a and Kdm6b in Regulation of Mammalian Neural Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  14. Article
  15. Single-Nuclei Sequencing Reveals a Robust Corticospinal Response to Nearby Axotomy But Overall Insensitivity to Spinal Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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  16. Review
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  20. Lipin1 depletion coordinates neuronal signaling pathways to promote motor and sensory axon regeneration after spinal cord injury.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article

91 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

11 authors at 3 institutions in 2 countries.

Stephane BelinF.M. Kirby Neurobiology Center, Boston Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.
Homaira NawabiF.M. Kirby Neurobiology Center, Boston Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.
Chen WangF.M. Kirby Neurobiology Center, Boston Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.
Shaojun TangDepartment of Pathology, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.
Alban LatremoliereF.M. Kirby Neurobiology Center, Boston Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.
Peter WarrenDepartment of Urology, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.
Hubert SchorleDepartment of Developmental Pathology, University of Bonn Medical School, Sigmund Freud Strasse 25, 53127 Bonn, Germany.
Ceren UncuF.M. Kirby Neurobiology Center, Boston Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.
Clifford J WoolfF.M. Kirby Neurobiology Center, Boston Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.
Zhigang HeF.M. Kirby Neurobiology Center, Boston Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA. Electronic address: zhigang.he@childrens.harvard.edu.
Judith A SteenF.M. Kirby Neurobiology Center, Boston Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA. Electronic address: judith.steen@childrens.harvard.edu.
Harvard University · USBoston Children's Hospital · USUniversity of Bonn · DE

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 Gabriel Kreiman · 1998 to 2026
$21.3M
SOCS3 and optic nerve regenerationR01EY021526 · NEI · BOSTON CHILDREN'S HOSPITAL · PI HE, ZHIGANG · 2011 to 2020
$4.1M
Regulation of SMN and Identification of its Downstream TargetR01NS066973 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI STEEN, JUDITH A · 2010 to 2014
$2.2M
Myopia: the role of cone opsin mutations & glasses that control axial elongationR01EY021242 · NEI · UNIVERSITY OF WASHINGTON · PI NEITZ, JAY · 2011 to 2015
$2.0M
New Approach to promote optic nerve regeneration and vision restorationR01EY021342 · NEI · BOSTON CHILDREN'S HOSPITAL · PI HE, ZHIGANG · 2011 to 2014
$1.7M
NEI NIH HHS EY021242NEI NIH HHS P30 EY012196NEI NIH HHS P30EY012196NEI NIH HHS R01 EY021242NEI NIH HHS R01 EY021342NEI NIH HHS R01 EY021526NICHD NIH HHS P30 HD018655NINDS NIH HHS NS066973NINDS NIH HHS R01 NS066973
6 · The paper itself

Abstract

Neurons differ in their responses to injury, but the underlying mechanisms remain poorly understood. Using quantitative proteomics, we characterized the injury-triggered response from purified intact and axotomized retinal ganglion cells (RGCs). Subsequent informatics analyses revealed a network of injury-response signaling hubs. In addition to confirming known players, such as mTOR, this also identified new candidates, such as c-myc, NFκB, and Huntingtin. Similar to mTOR, c-myc has been implicated as a key regulator of anabolic metabolism and is downregulated by axotomy. Forced expression of c-myc in RGCs, either before or after injury, promotes dramatic RGC survival and axon regeneration after optic nerve injury. Finally, in contrast to RGCs, neither c-myc nor mTOR was downregulated in injured peripheral sensory neurons. Our studies suggest that c-myc and other injury-responsive pathways are critical to the intrinsic regenerative mechanisms and might represent a novel target for developing neural repair strategies in adults.

Indexed as

ProteomicsAnimalsAxonsAxotomyCell SurvivalDisease Models, AnimalMice, Inbred C57BLMice, TransgenicNerve RegenerationNeuronsOptic NerveOptic Nerve InjuriesRetinal Ganglion CellsSignal Transduction

Identifiers

PMID25937169
PMCPMC4551425
OpenAlexW2028585054

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.