Evidence map›Paper›PMID 12545700›Full record

ArticleTransactions of the American Ophthalmological Society2002

Diabetes-induced dysfunction of retinal Müller cells.

Donald G Puro

Abstract read
In one paragraph

Article in Transactions of the American Ophthalmological Society, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

48 citing papers in PubMed, 90 citations in OpenAlex.

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  10. The innate immune system in diabetic retinopathy.Progress in retinal and eye research · 2021
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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

1 author.

Donald G PuroDepartments of Ophthalmology and Visual Sciences and Physiology, University of Michigan, Ann Arbor, USA.

Funding

NEI NIH HHS EY07003
6 · The paper itself

Abstract

purposeThis study tested the hypothesis that the function of the glutamate transporter in retinal Müller cells is compromised early in the course of diabetes by a mechanism involving oxidation. Dysfunction of this transporter, which removes glutamate from the extracellular space, may play a critical role in the disruption of glutamate homeostasis that occurs in the diabetic retina. Because glutamate is toxic to retinal neurons and is likely to exacerbate oxidative stress, elucidation of the mechanisms by which diabetes elevates the concentration of this amino acid may help to better understand the pathogenesis of diabetic retinopathy.

methodsMüller cells were freshly isolated from normal rats and those made diabetic by streptozotocin injection. The activity of the Müller cell glutamate transporter, which is electrogenic, was monitored via the perforated-patch configuration of the patch-clamp technique.

resultsFour weeks after the onset of hyperglycemia, dysfunction of the Müller cell glutamate transporter was detected (P = .005). After 13 weeks of streptozotocin-induced diabetes, the activity of this transporter was decreased by 67% (P = .001). Consistent with oxidation causing this dysfunction, exposure to a disulfide-reducing agent rapidly restored the activity of this transporter in Müller cells from diabetic retinas.

conclusionsSoon after the onset of experimental diabetes, the function of the glutamate transporter in Müller cells is decreased by a mechanism that is likely to involve oxidation. The demonstration that the activity of this transporter can be rapidly restored raises the possibility that targeting this molecule for therapeutic intervention may restore glutamate homeostasis and, thereby, ameliorate sight-threatening complications of diabetic retinopathy.

Indexed as

Amino Acid Transport System X-AGAnimalsDiabetes Mellitus, ExperimentalDiabetic RetinopathyElectrophysiologyGlutamic AcidHyperglycemiaNeurogliaOxidative StressPatch-Clamp TechniquesRatsRats, Long-EvansAmino Acid Transport System X-AGGlutamic Acid

Identifiers

PMID12545700
PMCPMC1358969
OpenAlexW2149104543

What OpenQuestion holds

Textmetadata
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.