Evidence map›Paper›PMID 41002420›Full record

ReviewCells2025

The Form and Function of Retinal Ganglion Cells in Diabetes.

Alistair J Barber

Abstract readReview
In one paragraph

Review in Cells, 2025. 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
–field-weighted citation impact
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.

  1. Review
  2. 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

1 author.

Alistair J BarberOphthalmology, and Cell & Biological Systems, Milton S. Hershey Medical Center, Penn State University College of Medicine, Room C4800, Mail code H166, 500 University Drive, Hershey, PA 17033, USA.

Funding

Unifying Mechanism of Oxidative Stress and Inflammation in AMDR21EY035844 · NEI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI DENNIS, MICHAEL D · 2024 to 2025
$460k
NEI NIH HHS R21 EY035844PHS/NIH-funded project 5R21EY035844-02
6 · The paper itself

Abstract

This review examines how diabetes affects the ganglion cells of the retina, including the axons that make up the optic nerve. Links between established changes in the morphology of retinal ganglion cells (RGCs) and vision loss, as well as other functions, such as the pupillary light reflex, are considered. RGC morphology and function are significantly altered in both animal models and humans with diabetes. Diabetes affects all parts of the RGC, including the dendrites, the cell body, the axons making up the nerve fiber layer, and the optic nerve. Subtypes of RGCs appear to be affected differently by diabetes, and the morphology and electrophysiological output are more significantly affected in ON-RGCs than in OFF cells, which may explain part of the mechanism underlying the widely documented diabetes-induced reduction in contrast sensitivity. Furthermore, the morphology of the specialized light-sensitive melanopsin-containing RGCs also appears to be affected by diabetes, which may explain deficits in circadian rhythm and the pupillary light reflex. Potential therapeutic approaches aimed at protecting RGCs in diabetes are also discussed. Overall, strong evidence supports the conclusion that diabetes impacts the form and function of RGCs and their axons within the optic nerve, resulting in deficient regulation of circadian rhythms and the pupillary light reflex, in addition to vision.

Indexed as

Diabetes MellitusRetinal Ganglion CellsAnimalsAxonsCircadian RhythmHumansOptic NerveReflex, Pupillaryapoptosiscontrast sensitivitymelanopsinnerve fiber layerneurodegenerationoptic nerve

Identifiers

PMID41002420
PMCPMC12468316

What OpenQuestion holds

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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.