Evidence map›Paper›PMID 34417332›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2021

Retinal Ganglion Cell Axon Regeneration Requires Complement and Myeloid Cell Activity within the Optic Nerve.

Sheri L Peterson, Yiqing Li, Christina J Sun, Kimberly A Wong, Kylie S Leung, Silmara de Lima, Nicholas J Hanovice, Kenya Yuki, Beth Stevens, Larry I Benowitz

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  15. The neuroimmune interface in retinal regeneration.Progress in retinal and eye research · 2025
    Review
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  17. Review
  18. Review
  19. Dual role of complement in neuronal repair.Frontiers in immunology · 2025
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 3 countries.

Sheri L PetersonLaboratories for Neuroscience Research in Neurosurgery Larry.Benowitz@childrens.harvard.edu Sheri.Peterson@childrens.harvard.edu.
Yiqing LiLaboratories for Neuroscience Research in Neurosurgery.
Christina J SunLaboratories for Neuroscience Research in Neurosurgery.
Kimberly A WongLaboratories for Neuroscience Research in Neurosurgery.
Kylie S LeungLaboratories for Neuroscience Research in Neurosurgery.
Silmara de LimaLaboratories for Neuroscience Research in Neurosurgery.
Nicholas J HanoviceLaboratories for Neuroscience Research in Neurosurgery.
Kenya YukiLaboratories for Neuroscience Research in Neurosurgery.
Beth StevensF.M. Kirby Neurobiology Center, and.ORCID 0000-0003-4226-1201
Larry I BenowitzLaboratories for Neuroscience Research in Neurosurgery Larry.Benowitz@childrens.harvard.edu Sheri.Peterson@childrens.harvard.edu.ORCID 0000-0002-0277-7222
Center for Neurosciences · USBroad Institute · USCenter for Children · USHarvard University · USSun Yat-sen University · CN

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI POMEROY, SCOTT LOREN · 1985 to 2015
$26.2M
Genetic Analysis and Manipulation Core (GAEC)P50HD105351 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI SCOTT Loren POMEROY, MUSTAFA SAHIN · 2021 to 2026
$9.4M
Training Program in the Molecular Bases of Eye DiseasesT32EY007145 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI Patricia Ann D'Amore, MEREDITH GREGORY-KSANDER · 1997 to 2026
$4.5M
An interneuronal signaling network governs the fate of retinal ganglion cells after optic nerve injuryR01EY027881 · NEI · BOSTON CHILDREN'S HOSPITAL · PI ROSENBERG, PAUL ALLEN · 2018 to 2022
$3.5M
NEI NIH HHS R01 EY027881NEI NIH HHS T32 EY007145NICHD NIH HHS P30 HD018655NICHD NIH HHS P50 HD105351
6 · The paper itself

Abstract

Axon regenerative failure in the mature CNS contributes to functional deficits following many traumatic injuries, ischemic injuries, and neurodegenerative diseases. The complement cascade of the innate immune system responds to pathogen threat through inflammatory cell activation, pathogen opsonization, and pathogen lysis, and complement is also involved in CNS development, neuroplasticity, injury, and disease. Here, we investigated the involvement of the classical complement cascade and microglia/monocytes in CNS repair using the mouse optic nerve injury (ONI) model, in which axons arising from retinal ganglion cells (RGCs) are disrupted. We report that central complement C3 protein and mRNA, classical complement C1q protein and mRNA, and microglia/monocyte phagocytic complement receptor CR3 all increase in response to ONI, especially within the optic nerve itself. Importantly, genetic deletion of

Indexed as

AnimalsAxonsComplement C1qComplement C3FemaleMaleMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMyeloid CellsNerve RegenerationOptic Nerve InjuriesRetinal Ganglion CellsComplement C1qComplement C3C1qC3CD11bCR3microgliamyelin

Identifiers

PMID34417332
PMCPMC8513703
OpenAlexW3194206769

What Socratic holds

Textmetadata
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.