Evidence map›Paper›PMID 38334594›Full record

ArticleCells2024

Synergistic Protection of Retinal Ganglion Cells (RGCs) by SARM1 Inactivation with CNTF in a Rodent Model of Nonarteritic Anterior Ischemic Optic Neuropathy.

Yan Guo, Zara Mehrabian, Jeffrey Milbrandt, Aaron DiAntonio, Steven L Bernstein

Open access · goldAbstract read
In one paragraph

Article in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.3field-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

5 citing papers in PubMed, 4 citations in OpenAlex.

  1. Hopx(+) optic nerve head-astrocytes counter neuronal stress and glaucoma damage.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Review
  4. Review
  5. Article
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

5 authors at 2 institutions in 1 country.

Yan GuoDepartments of Ophthalmology and Visual Sciences, School of Medicine, University of Maryland, Baltimore, MD 21201, USA.
Zara MehrabianDepartments of Ophthalmology and Visual Sciences, School of Medicine, University of Maryland, Baltimore, MD 21201, USA.
Jeffrey MilbrandtDepartment of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA.
Aaron DiAntonioNeedleman Center for Neurometabolism and Axonal Therapeutics, St. Louis, MO 63110, USA.
Steven L BernsteinDepartments of Ophthalmology and Visual Sciences, School of Medicine, University of Maryland, Baltimore, MD 21201, USA.ORCID 0000-0001-7758-0136
University of Maryland, Baltimore · USWashington University in St. Louis · US

Funding

DISSECTION OF SARM1-INDUCED AXON DEGENERATION AND CELL DEATHR01NS087632 · NINDS · WASHINGTON UNIVERSITY · PI Aaron Diantonio, JEFFREY D MILBRANDT · 2014 to 2026
$6.4M
Mechanisms of Optic Nerve Stroke NeuroprotectionR01EY015304 · NEI · UNIVERSITY OF MARYLAND BALTIMORE · PI BERNSTEIN, STEVEN L · 2004 to 2018
$4.7M
NEI NIH HHS R01 EY015304NIH HHS RO1 EY015404 to SLB and RO1 NS087632 to AD and JMNINDS NIH HHS R01 NS087632
6 · The paper itself

Abstract

We evaluated whether inhibiting sterile alpha and (Toll/interleukin receptor (TIR)) motif-containing 1 (SARM1) activity protects retinal ganglion cells (RGCs) following ischemic axonopathy (rodent nonarteritic anterior ischemic optic neuropathy: rNAION) by itself and combined with ciliary neurotrophic factor (CNTF). Genetically modified SARM1(-) rats were rNAION-induced in one eye and compared against equivalently induced wild-type animals of the same background. Optic nerve (ON) diameters were quantified using optical coherence tomography (SD-OCT). RGCs were quantified 30 d post-induction using retinal stereology for Brn3a(+) nuclei. ON sections were analyzed by TEM and immunohistochemistry. SARM1(-)(-) and WT animals were then bilaterally sequentially rNAION-induced. One eye received intravitreal vehicle injection following induction; the contralateral side received CNTF and was analyzed 30 d post-induction. Inhibiting SARM1 activity suppressed axonal collapse following ischemic axonopathy. SARM1(-) animals significantly reduced RGC loss, compared with WT animals (49.4 ± 6.8% RGC loss in SARM1(-) vs. 63.6 ± 3.2% sem RGC loss in WT; Mann-Whitney one-tailed U-test, (

Indexed as

Optic Neuropathy, IschemicRetinal Ganglion CellsAnimalsAnimals, WildArmadillo Domain ProteinsCiliary Neurotrophic FactorCytoskeletal ProteinsRatsRetinaRodentiaArmadillo Domain ProteinsCiliary Neurotrophic FactorCytoskeletal ProteinsSarm1 protein, rataxonopathyciliary neurotrophic factorischemianeuroprotectionnonarteritic anterior ischemic optic neuropathy (NAION)optic nerveretinal ganglion cellsrodentsterile alpha and (toll/interleukin receptor (TIR)) motif-containing 1 (SARM1)synergism

Identifiers

PMID38334594
PMCPMC10854792
OpenAlexW4391145281

What OpenQuestion 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 OpenQuestion graph.