Evidence map›Paper›PMID 37359418›Full record

ArticleMolecular therapy. Methods & clinical development2023

Human amnionic progenitor cell secretome mitigates the consequence of traumatic optic neuropathy in a mouse model.

Robyn McCartan, Arissa Gratkowski, Mackenzie Browning, Coral Hahn-Townsend, Scott Ferguson, Alexander Morin, Corbin Bachmeier, Andrew Pearson, Larry Brown, Michael Mullan and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Methods & clinical development, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Targeting dual specificity tyrosine-phosphorylation-regulated kinase 1A mitigates tauopathy and enhances recovery after repetitive head injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  2. 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

13 authors at 5 institutions in 1 country.

Robyn McCartanRoskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA.
Arissa GratkowskiRoskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA.
Mackenzie BrowningRoskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA.
Coral Hahn-TownsendRoskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA.
Scott FergusonRoskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA.
Alexander MorinRoskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA.
Corbin BachmeierRoskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA.
Andrew PearsonRoskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA.
Larry BrownNoveome Biotherapeutics, Inc., Pittsburgh, PA 15219, USA.
Michael MullanRoskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA.
Fiona CrawfordRoskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA.
Radouil TzekovUniversity of South Florida, Tampa, FL 33620, USA.
Benoit MouzonRoskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA.
Roskamp Institute · USJames A. Haley Veterans' Hospital · USBay Pines VA Healthcare System · USUniversity of Miami · USUniversity of South Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic optic neuropathy (TON) is a condition in which acute injury to the optic nerve from direct or indirect trauma results in vision loss. The most common cause of TON is indirect injury to the optic nerve caused by concussive forces that are transmitted to the optic nerve. TON occurs in up to 5% of closed-head trauma patients and there is currently no known effective treatment. One potential treatment option for TON is ST266, a cell-free biological solution containing the secretome of amnion-derived multipotent progenitor (AMP) cells. We investigated the efficacy of intranasal ST266 in a mouse model of TON induced by blunt head trauma. Injured mice treated with a 10-day regimen of ST266 showed an improvement in spatial memory and learning, a significant preservation of retinal ganglion cells, and a decrease in neuropathological markers in the optic nerve, optic tract, and dorsal lateral geniculate nucleus. ST266 treatment effectively downregulated the NLRP3 inflammasome-mediated neuroinflammation pathway after blunt trauma. Overall, treatment with ST266 was shown to improve functional and pathological outcomes in a mouse model of TON, warranting future exploration of ST266 as a cell-free therapeutic candidate for testing in all optic neuropathies.

Indexed as

mouse modelneurotraumaoptic nerve trauma,retinal ganglion cellssectretometraumatic brain injurytraumatic optic neuropathy

Identifiers

PMID37359418
PMCPMC10285248
OpenAlexW4366262988

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.