Evidence map›Paper›PMID 27163547›Full record

ReviewExperimental neurology2017

CNS repair and axon regeneration: Using genetic variation to determine mechanisms.

Andrea Tedeschi, Takao Omura, Michael Costigan

Abstract readReview
In one paragraph

Review in Experimental neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. In vivo programming of adult pericytes aids axon regeneration by providing cellular bridges for SCI repair.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  2. Review
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  5. Genes in Axonal Regeneration.Molecular neurobiology · 2024
    Review
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  20. Intrinsic mechanisms of neuronal axon regeneration.Nature reviews. Neuroscience · 2018
    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.

Andrea TedeschiGerman Center for Neurodegenerative Diseases (DZNE), 53175 Bonn, Germany. Electronic address: andrea.tedeschi@dzne.de.
Takao OmuraDepartment of Orthopaedic Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan. Electronic address: t.omura@hama-med.ac.jp.
Michael CostiganFM Kirby Neurobiology Center and Anesthesia Department, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA. Electronic address: michael.costigan@childrens.harvard.edu.

Funding

The mechanisms of action of T-lymphocytes in neuropathic painR01NS074430 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI COSTIGAN, MICHAEL · 2012 to 2016
$2.0M
NINDS NIH HHS R01 NS074430
6 · The paper itself

Abstract

The importance of genetic diversity in biological investigation has been recognized since the pioneering studies of Gregor Johann Mendel and Charles Darwin. Research in this area has been greatly informed recently by the publication of genomes from multiple species. Genes regulate and create every part and process in a living organism, react with the environment to create each living form and morph and mutate to determine the history and future of each species. The regenerative capacity of neurons differs profoundly between animal lineages and within the mammalian central and peripheral nervous systems. Here, we discuss research that suggests that genetic background contributes to the ability of injured axons to regenerate in the mammalian central nervous system (CNS), by controlling the regulation of specific signaling cascades. We detail the methods used to identify these pathways, which include among others Activin signaling and other TGF-β superfamily members. We discuss the potential of altering these pathways in patients with CNS damage and outline strategies to promote regeneration and repair by combinatorial manipulation of neuron-intrinsic and extrinsic determinants.

Indexed as

Central Nervous System DiseasesAnimalsAxonsGenetic VariationHumansNerve RegenerationSignal TransductionActivin/TGF-β signalingCAST/EiCNS regenerationCollaborative crossCongenicsGenetic backgroundNeuron-intrinsic and extrinsic factors

Identifiers

PMID27163547
PMCPMC5097896

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.