Evidence map›Paper›PMID 37895039›Full record

ReviewInternational journal of molecular sciences2023

Inflammatory Mediators of Axon Regeneration in the Central and Peripheral Nervous Systems.

Larry I Benowitz, Lili Xie, Yuqin Yin

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Disruption of G3BP1 granules promotes mammalian CNS and PNS axon regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. 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 2 countries.

Larry I BenowitzDepartment of Neurosurgery, Boston Children's Hospital, Boston, MA 02115, USA.
Lili XieDepartment of Neurosurgery, Boston Children's Hospital, Boston, MA 02115, USA.
Yuqin YinDepartment of Neurosurgery, Boston Children's Hospital, Boston, MA 02115, USA.ORCID 0000-0002-0980-6954
Boston Children's Hospital · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI WOOLF, CLIFFORD J · 1985 to 2015
$26.2M
Viral ModuleP30EY012196 · NEI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI MARGARET S LIVINGSTONE · 1998 to 2026
$21.3M
Genetic Analysis and Manipulation Core (GAEC)P50HD105351 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI Hisashi Umemori · 2021 to 2026
$9.4M
MOLECULAR BASES OF NEURONAL CONNECTIVITYR01EY005690 · NEI · MC LEAN HOSPITAL (BELMONT, MA) · PI BENOWITZ, LARRY IRA · 1985 to 2012
$4.7M
Zinc is a critical regulator of cell death and axon regeneration after CNS injuryR01EY024481 · NEI · BOSTON CHILDREN'S HOSPITAL · PI BENOWITZ, LARRY IRA, ROSENBERG, PAUL ALLEN · 2015 to 2019
$2.8M
Novel growth factors and regenerative RGC subtypes for optic nerve regenerationR21EY033550 · NEI · BOSTON CHILDREN'S HOSPITAL · PI YIN, YUQIN · 2023 to 2024
$487k
NEI NIH HHS P30 EY012196NEI NIH HHS R01 EY005690NEI NIH HHS R01 EY024481NEI NIH HHS R21 EY033550NICHD NIH HHS P30 HD018655NICHD NIH HHS P50 HD105351
6 · The paper itself

Abstract

Although most pathways in the mature central nervous system cannot regenerate when injured, research beginning in the late 20th century has led to discoveries that may help reverse this situation. Here, we highlight research in recent years from our laboratory identifying oncomodulin (Ocm), stromal cell-derived factor (SDF)-1, and chemokine CCL5 as growth factors expressed by cells of the innate immune system that promote axon regeneration in the injured optic nerve and elsewhere in the central and peripheral nervous systems. We also review the role of ArmC10, a newly discovered Ocm receptor, in mediating many of these effects, and the synergy between inflammation-derived growth factors and complementary strategies to promote regeneration, including deleting genes encoding cell-intrinsic suppressors of axon growth, manipulating transcription factors that suppress or promote the expression of growth-related genes, and manipulating cell-extrinsic suppressors of axon growth. In some cases, combinatorial strategies have led to unprecedented levels of nerve regeneration. The identification of some similar mechanisms in human neurons offers hope that key discoveries made in animal models may eventually lead to treatments to improve outcomes after neurological damage in patients.

Indexed as

AxonsNerve RegenerationAnimalsCentral Nervous SystemHumansIntercellular Signaling Peptides and ProteinsNeuronsOptic NerveIntercellular Signaling Peptides and ProteinsArmC10axon regenerationCCL5conditioning lesiongrowth factorsinflammatory cellsoncomodulinSDF1

Identifiers

PMID37895039
PMCPMC10607492
OpenAlexW4387780532

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.