Evidence map›Paper›PMID 30249212›Full record

ArticleBMC ophthalmology2018

Metabolic memory in mitochondrial oxidative damage triggers diabetic retinopathy.

Zhaoge Wang, Haixia Zhao, Wenying Guan, Xin Kang, Xue Tai, Ying Shen

Open access · goldAbstract read
In one paragraph

Article in BMC ophthalmology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. mRNAs expression profiles of high glucose-induced memory in human umbilical vein endothelial cells.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019
    Article
  16. Article
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 1 institution in 1 country.

Zhaoge WangCenter of Myopia, the Affiliated Hospital of Inner Mongolia Medical University, 1 Tongdao North Street, Hohhot, 010050, China.
Haixia ZhaoCenter of Myopia, the Affiliated Hospital of Inner Mongolia Medical University, 1 Tongdao North Street, Hohhot, 010050, China.
Wenying GuanCenter of Myopia, the Affiliated Hospital of Inner Mongolia Medical University, 1 Tongdao North Street, Hohhot, 010050, China.
Xin KangCenter of Myopia, the Affiliated Hospital of Inner Mongolia Medical University, 1 Tongdao North Street, Hohhot, 010050, China.
Xue TaiCenter of Myopia, the Affiliated Hospital of Inner Mongolia Medical University, 1 Tongdao North Street, Hohhot, 010050, China.
Ying ShenCenter of Myopia, the Affiliated Hospital of Inner Mongolia Medical University, 1 Tongdao North Street, Hohhot, 010050, China. 2438413496@qq.com.
Inner Mongolia Medical University · CN

Funding

Natural Science Foundation of Inner Mongolia Autonomous Region, China 2011MS1137Research Funds of the Affiliated Hospital of Inner Mongolia Medical University NYFYYB2014020
6 · The paper itself

Abstract

backgroundDiabetic retinopathy (DR) is a microvascular complication induced by high blood glucose. This study was conducted to investigate the effect of metabolic memory on mitochondrial oxidative damage-induced DR.

methodsRat retinal endothelial cells (rRECs) were isolated from SD rats and treated with high glucose (20 mM) for various times and then cultured in normal glucose (5.6 mM) medium for 2 days. The cells were assayed for the expression of respiratory chain complexes cytochrome c oxidase subunit 1 (CO1) and NADPH-1 using RT-PCR, mitochondrial membrane potentials and reactive oxygen species (ROS) production using flow cytometry and apoptosis using Annexin V/PI flow cytometry.

resultsrRECs displayed like short spindles after cultured for 9-10 days and reached 100% confluency. Compared with the control grown in normal glucose (5.6 mM) medium, rRECs exposed to high glucose medium for 3, 12 and 24 h had significantly increased mRNA levels of CO1 and NAPDH-1 even after being shifted back to normal glucose medium. They also had lower mitochondrial membrane potential (89.13% vs 78.21%, p < 0.05), cytochrome C level (1 in control vs 0.25 after 24 h exposure to high glucose, p < 0.05 and higher ROS production (2.77% in control vs 9.00% after 12 h exposure to high glucose, p < 0.05) and apoptosis (7.15% in control vs and 29.91% after 24 h exposure to high glucose, p < 0.05).

conclusionIt is likely that mitochondrial oxidative damage triggers metabolic memory via ROS overproduction, leading to diabetic retinopathy.

Indexed as

AnimalsApoptosisCells, CulturedDiabetic RetinopathyElectron Transport Complex IVEndothelial CellsGlucoseHumansMembrane Potential, MitochondrialMitochondriaNADPOxidative StressRatsRats, Sprague-DawleyReactive Oxygen SpeciesElectron Transport Complex IVGlucoseNADPReactive Oxygen SpeciesApoptosisDiabetic retinopathyMetabolic memoryMitochondriaROS

Identifiers

PMID30249212
PMCPMC6154827
OpenAlexW2890735692

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.