Evidence map›Paper›PMID 25192646›Full record

ReviewBrain research2015

Molecular mechanisms of scar-sourced axon growth inhibitors.

Yosuke Ohtake, Shuxin Li

Open access · greenAbstract readReview
In one paragraph

Review in Brain research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

57 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. The Repair Manual of a Fruit Fly Brain.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Article
  5. Article
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  7. Repair mechanisms of the central nervous system: From axon sprouting to remyelination.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  8. Article
  9. Review
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  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Extracellular Matrix in Neural Plasticity and Regeneration.Cellular and molecular neurobiology · 2022
    Review
  17. Review
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Yosuke OhtakeShriners Hospitals Pediatric Research Center and Department of Anatomy and Cell Biology, Temple University School of Medicine, 3500N. Broad Street, Philadelphia 19140, PA, USA.
Shuxin LiShriners Hospitals Pediatric Research Center and Department of Anatomy and Cell Biology, Temple University School of Medicine, 3500N. Broad Street, Philadelphia 19140, PA, USA. Electronic address: Shuxin.li@temple.edu.
Temple University · US

Funding

CSPG receptors and PTEN in CNS regenerationR01NS079432 · NINDS · TEMPLE UNIV OF THE COMMONWEALTH · PI LI, SHUXIN · 2014 to 2018
$1.7M
Therapeutic Strategies for Repairing Optic Nerve InjuryR01EY024575 · NEI · TEMPLE UNIV OF THE COMMONWEALTH · PI LI, SHUXIN · 2014 to 2017
$1.4M
Overcoming glial scar inhibitions on axonal growthR21NS066114 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LI, SHUXIN · 2010 to 2011
$432k
NEI NIH HHS R01 EY024575NINDS NIH HHS 1R01NS079432NINDS NIH HHS 1R21NS066114NINDS NIH HHS R01 NS079432NINDS NIH HHS R21 NS066114
6 · The paper itself

Abstract

Astrogliosis is a defense response of the CNS to minimize primary damage and to repair injured tissues, but it ultimately generates harmful effects by upregulating inhibitory molecules to suppress neuronal elongation and forming potent barriers to axon regeneration. Chondroitin sulfate proteoglycans (CSPGs) are highly expressed by reactive scars and are potent contributors to the non-permissive environment in mature CNS. Surmounting strong inhibition by CSPG-rich scar is an important therapeutic goal for achieving functional recovery after CNS injuries. Currently, enzymatic digestion of CSPGs with locally applied chondroitinase ABC is the main in vivo approach to overcome scar inhibition, but several disadvantages may prevent using this bacterial enzyme as a therapeutic option for patients. A better understanding of molecular mechanisms underlying CSPG function may facilitate development of new effective therapies to overcome scar-mediated inhibition. Previous studies support that CSPGs act by non-specifically hindering the binding of matrix molecules to their cell surface receptors through steric interactions, but two members of the leukocyte common antigen related (LAR) phosphatase subfamily, protein tyrosine phosphatase σ and LAR, are functional receptors that bind CSPGs with high affinity and mediate CSPG inhibition. CSPGs may also act by binding two receptors for myelin-associated growth inhibitors, Nogo receptors 1 and 3. Thus, CSPGs inhibit axon growth through multiple mechanisms, making them especially potent and difficult therapeutic targets. Identification of CSPG receptors is not only important for understanding the scar-mediated growth suppression, but also for developing novel and selective therapies to promote axon sprouting and/or regeneration after CNS injuries. This article is part of a Special Issue entitled SI: Spinal cord injury.

Indexed as

AnimalsAstrocytesAxonsChondroitin ABC LyaseChondroitin Sulfate ProteoglycansCicatrixGliosisGrowth InhibitorsHumansNerve RegenerationReceptor-Like Protein Tyrosine Phosphatases, Class 2Receptors, Cell SurfaceSignal TransductionChondroitin ABC LyaseChondroitin Sulfate ProteoglycansGrowth InhibitorsReceptor-Like Protein Tyrosine Phosphatases, Class 2Receptors, Cell SurfaceAstrogliosisAxon regenerationCNS injuryCSPG receptorLARNogo receptorPTPσReactive astrocyteScar

Identifiers

PMID25192646
PMCPMC4345149
OpenAlexW2035943609

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.