Evidence map›Paper›PMID 29352075›Full record

ReviewClinical science (London, England : 1979)2018

O-Linked β-

Zafer Gurel, Nader Sheibani

Abstract readReview
In one paragraph

Review in Clinical science (London, England : 1979), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
–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

32 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Diabetic Retinopathy-A Review.Current diabetes reviews · 2025
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Multi-omics in exploring the pathophysiology of diabetic retinopathy.Frontiers in cell and developmental biology · 2024
    Review
  13. Review
  14. O-GlcNAcylation in ischemic diseases.Frontiers in pharmacology · 2024
    Review
  15. Review
  16. Article
  17. Proteomic analysis of diabetic retinas.Frontiers in endocrinology · 2023
    Article
  18. Review
  19. Metabolites · 2022
    Review
  20. Cells · 2022
    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

2 authors.

Zafer GurelDepartments of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705, U.S.A. zgurel@wisc.edu.
Nader SheibaniDepartments of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705, U.S.A.

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Christian Capitini · 1985 to 2026
$142.6M
UW Vision Research Core - Administrative CoreP30EY016665 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI Donna M Peters · 2005 to 2026
$12.6M
Novel Antiangiogenic Peptides for Treatment of Exudative AMDR24EY022883 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI SHEIBANI, NADER · 2013 to 2017
$6.2M
Investigating oxygen metabolism in diabetic retinopathyR01EY026078 · NEI · NORTHWESTERN UNIVERSITY · PI SHEIBANI, NADER, ZHANG, HAO F · 2016 to 2020
$2.3M
NCI NIH HHS P30 CA014520NEI NIH HHS P30 EY016665NEI NIH HHS R01 EY026078NEI NIH HHS R24 EY022883
6 · The paper itself

Abstract

The incidence of diabetes continues to rise among all ages and ethnic groups worldwide. Diabetic retinopathy (DR) is a complication of diabetes that affects the retinal neurovasculature causing serious vision problems, including blindness. Its pathogenesis and severity is directly linked to the chronic exposure to high glucose conditions. No treatments are currently available to stop the development and progression of DR. To develop new and effective therapeutic approaches, it is critical to better understand how hyperglycemia contributes to the pathogenesis of DR at the cellular and molecular levels. We propose alterations in O-GlcNAc modification of target proteins during diabetes contribute to the development and progression of DR. The O-GlcNAc modification is regulated through hexosamine biosynthetic pathway. We showed this pathway is differentially activated in various retinal vascular cells under high glucose conditions perhaps due to their selective metabolic activity. O-GlcNAc modification can alter protein stability, activity, interactions, and localization. By targeting the same amino acid residues (serine and threonine) as phosphorylation, O-GlcNAc modification can either compete or cooperate with phosphorylation. Here we will summarize the effects of hyperglycemia-induced O-GlcNAc modification on the retinal neurovasculature in a cell-specific manner, providing new insight into the role of O-GlcNAc modification in early loss of retinal pericytes and the pathogenesis of DR.

Indexed as

Protein Processing, Post-TranslationalAcetylglucosamineAnimalsDiabetic RetinopathyGlucoseHumansHyperglycemiaPericytesRetinaSignal TransductionAcetylglucosamineGlucosediabetesdiabetic retinopathyhyperglycemiaO-GlcNAcpost translational modification

Identifiers

PMID29352075
PMCPMC6016849

What OpenQuestion holds

Textmetadata
LicenceTDM
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.