Evidence map›Paper›PMID 28586916›Full record

ArticleInvestigative ophthalmology & visual science2017

High Glucose Induces Mitochondrial Dysfunction in Retinal Müller Cells: Implications for Diabetic Retinopathy.

Thomas Tien, Joyce Zhang, Tetsuya Muto, Dongjoon Kim, Vijay P Sarthy, Sayon Roy

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

66 citing papers in PubMed, 119 citations in OpenAlex.

  1. Regulation of Glutathione Peroxidase 4 in Diabetic Retinopathy.International journal of molecular sciences · 2026
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  6. Mitochondrial Fragmentation and Long Noncoding RNAInternational journal of molecular sciences · 2025
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6 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Thomas TienDepartments of Medicine and Ophthalmology, Boston University School of Medicine, Boston, Massachusetts, United States.
Joyce ZhangDepartments of Medicine and Ophthalmology, Boston University School of Medicine, Boston, Massachusetts, United States.
Tetsuya MutoDepartments of Medicine and Ophthalmology, Boston University School of Medicine, Boston, Massachusetts, United States.
Dongjoon KimDepartments of Medicine and Ophthalmology, Boston University School of Medicine, Boston, Massachusetts, United States.
Vijay P SarthyDepartment of Ophthalmology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States.
Sayon RoyDepartments of Medicine and Ophthalmology, Boston University School of Medicine, Boston, Massachusetts, United States.
Boston University · USNorthwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: To investigate whether high glucose (HG) induces mitochondrial dysfunction and promotes apoptosis in retinal Müller cells. Methods: Rat retinal Müller cells (rMC-1) grown in normal (N) or HG (30 mM glucose) medium for 7 days were subjected to MitoTracker Red staining to identify the mitochondrial network. Digital images of mitochondria were captured in live cells under confocal microscopy and analyzed for mitochondrial morphology changes based on form factor (FF) and aspect ratio (AR) values. Mitochondrial metabolic function was assessed by measuring oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) using a bioenergetic analyzer. Cells undergoing apoptosis were identified by differential dye staining and TUNEL assay, and cytochrome c levels were assessed by Western blot analysis. Results: Cells grown in HG exhibited significantly increased mitochondrial fragmentation compared to those grown in N medium (FF = 1.7 ± 0.1 vs. 2.3 ± 0.1; AR = 2.1 ± 0.1 vs. 2.5 ± 0.2; P < 0.01). OCR and ECAR were significantly reduced in cells grown in HG medium compared to those grown in N medium (steady state: 75% ± 20% of control, P < 0.02; 64% ± 22% of control, P < 0.02, respectively). These cells also exhibited a significant increase (∼2-fold) in the number of apoptotic cells compared to those grown in N medium (P < 0.01), with a concomitant increase in cytochrome c levels (247% ± 94% of control, P < 0.05). Conclusions: Findings indicate that HG-induced mitochondrial morphology changes and subsequent mitochondrial dysfunction may contribute to retinal Müller cell loss associated with diabetic retinopathy.

Indexed as

ApoptosisDiabetes Mellitus, ExperimentalAnimalsBlotting, WesternCells, CulturedDiabetic RetinopathyDose-Response Relationship, DrugEnergy MetabolismEpendymoglial CellsGlucoseIn Situ Nick-End LabelingMicroscopy, ConfocalMitochondriaRatsGlucose

Identifiers

PMID28586916
PMCPMC5460955
OpenAlexW2621958502

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.