Evidence map›Paper›PMID 34232257›Full record

ArticleInvestigative ophthalmology & visual science2021

Diabetes Exacerbates the Intraocular Pressure-Independent Retinal Ganglion Cells Degeneration in the DBA/2J Model of Glaucoma.

Rosario Amato, Francesca Lazzara, Tsung-Han Chou, Giovanni Luca Romano, Maurizio Cammalleri, Massimo Dal Monte, Giovanni Casini, Vittorio Porciatti

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.4field-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

23 citing papers in PubMed, 28 citations in OpenAlex.

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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

8 authors at 3 institutions in 2 countries.

Rosario AmatoDepartment of Biology, University of Pisa, Pisa, Italy.
Francesca LazzaraBascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, Florida, United States.
Tsung-Han ChouBascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, Florida, United States.
Giovanni Luca RomanoBascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, Florida, United States.
Maurizio CammalleriDepartment of Biology, University of Pisa, Pisa, Italy.
Massimo Dal MonteDepartment of Biology, University of Pisa, Pisa, Italy.
Giovanni CasiniDepartment of Biology, University of Pisa, Pisa, Italy.
Vittorio PorciattiBascom Palmer Eye Institute, Miller School of Medicine, University of Miami, Miami, Florida, United States.
University of Pisa · ITUniversity of Miami · USUniversity of Catania · IT

Funding

Shared Equipment ModuleP30EY014801 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Victor L Perez · 2004 to 2026
$12.2M
RETINAL GANGLION CELL PLASTICITY IN GLAUCOMAR01EY019077 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI PORCIATTI, VITTORIO · 2009 to 2015
$2.1M
NEI NIH HHS P30 EY014801NEI NIH HHS R01 EY019077
6 · The paper itself

Abstract

Purpose: Glaucoma is a multifactorial disease, causing retinal ganglion cells (RGCs) and optic nerve degeneration. The role of diabetes as a risk factor for glaucoma has been postulated but still not unequivocally demonstrated. The purpose of this study is to clarify the effect of diabetes in the early progression of glaucomatous RGC dysfunction preceding intraocular pressure (IOP) elevation, using the DBA/2J mouse (D2) model of glaucoma. Methods: D2 mice were injected with streptozotocin (STZ) obtaining a combined model of diabetes and glaucoma (D2 + STZ). D2 and D2 + STZ mice were monitored for weight, glycemia, and IOP from 3.5 to 6 months of age. In addition, the activity of RGC and outer retina were assessed using pattern electroretinogram (PERG) and flash electroretinogram (FERG), respectively. At the end point, RGC density and astrogliosis were evaluated in flat mounted retinas. In addition, Müller cell reactivity was evaluated in retinal cross-sections. Finally, the expression of inflammation and oxidative stress markers were analyzed. Results: IOP was not influenced by time or diabetes. In contrast, RGC activity resulted progressively decreased in the D2 group independently from IOP elevation and outer retinal dysfunction. Diabetes exacerbated RGC dysfunction, which resulted independent from variation in IOP and outer retinal activity. Diabetic retinas displayed decreased RGC density and increased glial reactivity given by an increment in oxidative stress and inflammation. Conclusions: Diabetes can act as an IOP-independent risk factor for the early progression of glaucoma promoting oxidative stress and inflammation-mediated RGC dysfunction, glial reactivity, and cellular death.

Indexed as

AnimalsAxonsDiabetes Mellitus, ExperimentalElectroretinographyGlaucomaIntraocular PressureMiceMice, Inbred DBARetinaRetinal Ganglion Cells

Identifiers

PMID34232257
PMCPMC8267218
OpenAlexW3178644008

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.