Evidence map›Paper›PMID 24260294›Full record

ArticlePloS one2013

RETRACTED: High glucose induced oxidative stress and apoptosis in cardiac microvascular endothelial cells are regulated by FoxO3a.

Chaoming Peng, Junli Ma, Xue Gao, Peng Tian, Wenzhang Li, Lei Zhang

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. NADPH Oxidases, Angiogenesis, and Peripheral Artery Disease.Antioxidants (Basel, Switzerland) · 2017
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Chaoming PengDepartment of General Internal Medicine, The First Affiliated Hospital of Chengdu Medicine College, Chengdu, China.
Junli Ma
Xue Gao
Peng Tian
Wenzhang Li
Lei Zhang
First Affiliated Hospital of Chengdu Medical College · CN302 Military Hospital of China · CNThe Military General Hospital of Beijing PLA · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimCardiac microvascular endothelial cells (CMECs) dysfunction contributes to cardiovascular complications in diabetes, whereas, the underlying mechanism is not fully clarified. FoxO transcription factors are involved in apoptosis and reactive oxygen species (ROS) production. Therefore, the present study was designed to elucidate the potential role of FoxO3a on the CMECs injury induced by high glucose. MATERIALS AND

methodsCMECs were isolated from hearts of adult rats and cultured in normal or high glucose medium for 6 h, 12 h and 24 h respectively. To down-regulate FoxO3a expression, CMECs were transfected with FoxO3a siRNA. ROS accumulation and apoptosis in CMECs were assessed by dihydroethidine (DHE) staining and TUNEL assay respectively. Moreover, the expressions of Akt, FoxO3a, Bim and BclxL in CMECs were assessed by Western blotting assay.

resultsROS accumulation in CMECs was significantly increased after high glucose incubation for 6 to 24 h. Meanwhile, high glucose also increased apoptosis in CMECs, correlated with decreased the phosphorylation expressions of Akt and FoxO3a. Moreover, high glucose incubation increased the expression of Bim, whereas increased anti-apoptotic protein BclxL. Furthermore, siRNA target FoxO3a silencing enhanced the ROS accumulation, whereas suppressed apoptosis in CMECs. FoxO3a silencing also abolished the disturbance of Bcl-2 proteins induced by high glucose in CMECs.

conclusionOur data provide evidence that high glucose induced FoxO3a activation which suppressed ROS accumulation, and in parallel, resulted in apoptosis of CMECs.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11bcl-X ProteinDown-RegulationEndothelial CellsEndothelium, VascularForkhead Box Protein O3Forkhead Transcription FactorsGlucoseHeartMaleMembrane ProteinsMicrovesselsOxidative StressApoptosis Regulatory ProteinsBcl2l11 protein, ratBcl2l1 protein, ratBcl-2-Like Protein 11bcl-X ProteinForkhead Box Protein O3Forkhead Transcription FactorsFOXO3 protein, ratGlucoseMembrane ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesRNA, Small Interfering

Identifiers

PMID24260294
PMCPMC3832590
OpenAlexW2024395853

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.