RAGE and its ligand amyloid beta promote retinal ganglion cell loss following ischemia-reperfusion injury.

Nafiseh Seyed Hosseini Fin, Dana Georgevsky, Maria B Sukkar, S Mojtaba Golzan

Open access · goldAbstract read

In one paragraph

Article in Frontiers in cellular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing papers in PubMed

0.6field-weighted citation impact, top 36% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

Neurotoxic β-amyloid oligomers cause mitochondrial dysfunction-the trigger for PANoptosis in neurons.Frontiers in aging neuroscience · 2024
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

4 authors at 1 institution in 1 country.

Nafiseh Seyed Hosseini FinVision Science Group, Graduate School of Health, University of Technology Sydney, Sydney, NSW, Australia.

Dana GeorgevskyVision Science Group, Graduate School of Health, University of Technology Sydney, Sydney, NSW, Australia.

Maria B SukkarPharmacy Discipline, Graduate School of Health, University of Technology Sydney, Sydney, NSW, Australia.

S Mojtaba GolzanVision Science Group, Graduate School of Health, University of Technology Sydney, Sydney, NSW, Australia.

University of Technology Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Glaucoma is a progressive neurodegenerative disease associated with age. Accumulation of amyloid-beta (Aß) proteins in the ganglion cell layer (GCL) and subsequent retinal ganglion cell (RGC) loss is an established pathological hallmark of the disease. The mechanism through which Aß provokes RGC loss remains unclear. The receptor for the advanced glycation end product (RAGE), and its ligand Aß, have been shown to mediate neuronal loss Methods: Retinal ischemia was induced by an acute elevation of intraocular pressure in RAGE Results: Retinal ischemia resulted in 1.9-fold higher RGC loss in WT mice compared to RAGE Discussion: RAGE

Indexed as

amyloid betaglaucomareceptor for advanced glycation end productsretinal ganglion cell lossretinal ischemia-reperfusion

Identifiers

PMID37124398

DOI10.3389/fncel.2023.1156084

PMCPMC10130520

OpenAlexW4365142396

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.