Evidence map›Paper›PMID 26717002›Full record

ArticlePediatric research2016

Gestational diabetes induces alterations of sirtuins in fetal endothelial cells.

Juan Gui, Arne Potthast, Anne Rohrbach, Katja Borns, Anibh M Das, Frauke von Versen-Höynck

Open access · bronzeAbstract read
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In one paragraph

Article in Pediatric research, 2016. 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
0.6field-weighted citation impact, top 26% 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, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Impaired Angiogenic Function of Fetal Endothelial Progenitor Cells viaInternational journal of molecular sciences · 2023
    Article
  6. Review
  7. The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022
    Review
  8. Article
  9. Advances in the role of silence information regulator family in pathological pregnancy.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. 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

6 authors at 2 institutions in 2 countries.

Juan GuiDepartment of Obstetrics and Gynecology, Hannover Medical School, Hannover, Germany.
Arne PotthastDepartment of Pediatrics, Hannover Medical School, Hannover, Germany.
Anne RohrbachDepartment of Obstetrics and Gynecology, Hannover Medical School, Hannover, Germany.
Katja BornsDepartment of Obstetrics and Gynecology, Hannover Medical School, Hannover, Germany.
Anibh M DasDepartment of Pediatrics, Hannover Medical School, Hannover, Germany.
Frauke von Versen-HöynckDepartment of Obstetrics and Gynecology, Hannover Medical School, Hannover, Germany.
Medizinische Hochschule Hannover · DETongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGestational diabetes (GDM) has long-term consequences for the offspring. Sirtuins (SIRTs) are associated with vascular and metabolic functions. We studied the impact of GDM on SIRT activity and expression in fetal endothelial colony-forming cells (ECFCs) and human umbilical vein endothelial cells (HUVECs) from pregnancies complicated by GDM.

methodsECFCs and HUVECs were isolated from cord and cord blood of 10 uncomplicated pregnancies (NPs) and 10 GDM pregnancies. Nicotinamidadenindinukleotid (NAD(+)) concentration, SIRT1 and SIRT3 activity, transcription levels of SIRT1, SIRT3, and SIRT4, and protein levels of SIRT1, SIRT3, and SIRT4 were determined in vitro with or without SIRT activators resveratrol (RSV) and paeonol.

resultsFetal ECFCs from GDM pregnancies showed a decreased NAD(+) concentration, reduced SIRT1 and SIRT3 activity, and lower transcription levels of SIRT1, SIRT3, and SIRT4. HUVECs from GDM pregnancies had decreased NAD(+) concentrations and transcription levels of SIRT1 and SIRT4. RSV markedly enhanced the expression and activity of SIRTs in ECFCs and HUVECs, while paeonol was active only in ECFCs.

conclusionA reduction of SIRT activity and expression in fetal endothelial cells provides potential mechanistic insights into the pathophysiology of long-term cardiovascular complications observed in the offspring of GDM pregnancies. SIRT activators can increase SIRT activity in ECFCs, which opens perspectives for new therapeutic targets.

Indexed as

AdultBody Mass IndexDiabetes, GestationalEndothelial CellsFemaleGene Expression RegulationHemoglobinsHumansHuman Umbilical Vein Endothelial CellsInfant, NewbornMaleMitochondrial ProteinsNADPregnancySirtuin 1Sirtuin 3HemoglobinsMitochondrial ProteinsNADSIRT1 protein, humanSIRT3 protein, humanSIRT4 protein, humanSirtuin 1Sirtuin 3Sirtuins

Identifiers

PMID26717002
OpenAlexW2268709907

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.