Evidence map›Paper›PMID 39384641›Full record

ArticlePflugers Archiv : European journal of physiology2025

Characterization of human placental fetal vessels in gestational diabetes mellitus.

Philine S Carstens, Heike Brendel, M Leyre Villar-Ballesteros, Jennifer Mittag, Clara Hengst, Coy Brunssen, Cahit Birdir, Paul D Taylor, Lucilla Poston, Henning Morawietz

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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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

  1. Pooled it
  2. Ferroptosis-Mediated Placental Dysfunction in the Pathophysiology of Gestational Diabetes Mellitus.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
    Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Philine S Carstens *Division of Vascular Endothelium and Microcirculation, Department of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus, TUD Dresden University of Technology, Fetscherstr. 74, 01307, Dresden, Germany.
Heike Brendel *Division of Vascular Endothelium and Microcirculation, Department of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus, TUD Dresden University of Technology, Fetscherstr. 74, 01307, Dresden, Germany.ORCID 0000-0003-1214-1807
M Leyre Villar-BallesterosDivision of Vascular Endothelium and Microcirculation, Department of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus, TUD Dresden University of Technology, Fetscherstr. 74, 01307, Dresden, Germany.
Jennifer MittagDivision of Vascular Endothelium and Microcirculation, Department of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus, TUD Dresden University of Technology, Fetscherstr. 74, 01307, Dresden, Germany.
Clara HengstDivision of Vascular Endothelium and Microcirculation, Department of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus, TUD Dresden University of Technology, Fetscherstr. 74, 01307, Dresden, Germany.
Coy BrunssenDivision of Vascular Endothelium and Microcirculation, Department of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus, TUD Dresden University of Technology, Fetscherstr. 74, 01307, Dresden, Germany.
Cahit BirdirDepartment of Obstetrics and Gynecology, Faculty of Medicine and University Hospital Carl Gustav Carus, TUD Dresden University of Technology, Dresden, Germany.
Paul D TaylorDepartment of Women & Children's Health, School of Life Course & Population Sciences, King's College London, London, UK.
Lucilla PostonDepartment of Women & Children's Health, School of Life Course & Population Sciences, King's College London, London, UK.ORCID 0000-0003-1100-2821
Henning MorawietzDivision of Vascular Endothelium and Microcirculation, Department of Medicine III, Faculty of Medicine and University Hospital Carl Gustav Carus, TUD Dresden University of Technology, Fetscherstr. 74, 01307, Dresden, Germany. Henning.Morawietz@tu-dresden.de.ORCID 0000-0001-9360-9736

Funding

Deutsche Forschungsgemeinschaft 288034826 - IRTG 2251Faculty of Medicine Carl Gustav Carus of TUD Dresden University of Technology Carus PromotionskollegTUD Dresden University of Technology Open Access Funding by Publication Fund
6 · The paper itself

Abstract

Gestational diabetes mellitus is one of the most common complications during pregnancy. Its prevalence is rapidly increasing worldwide. Gestational diabetes mellitus is leading to an elevated risk for the development of endothelial dysfunction and cardiovascular diseases both in the mother and the child in later life. The underlying pathophysiological mechanisms are not well-understood. Therefore, we aimed to characterize the endothelial function in fetal placental vessels from mothers with gestational diabetes mellitus. In this study, we distinguished between insulin-treated and diet-controlled gestational diabetes mothers and compared them to a normoglycemic control group. The clinical data confirmed pre-conceptional overweight as a risk factor in women with insulin-treated gestational diabetes mellitus. The insulin-treated gestational diabetes group was also characterized by a recent family history of diabetes compared to mothers of the control or diet-controlled gestational diabetes group. Analyses of blood serum from umbilical cords suggested a reduced fetal insulin metabolism in the insulin-treated gestational diabetes group. Vascular function analysis in fetal placental vessels revealed an altered substance P-induced vasorelaxation in vessels from patients with insulin-dependent gestational diabetes. Inhibition of nitric oxide synthase affected only fetal vessel segments from the control group or diet-controlled gestational diabetes group, but not from insulin-dependent gestational diabetes. Finally, we found a significantly decreased substance P receptor (TACR1) mRNA expression in fetal vessel segments from patients with insulin-treated gestational diabetes. In conclusion, we provide evidence that different pathophysiological mechanisms might be responsible for the development of insulin-treated versus diet-controlled gestational diabetes. Only in fetal vessels from patients with insulin-treated gestational diabetes were we able to detect an endothelial dysfunction and a reduced fetal insulin conversion. This provides novel insights into the pathophysiology of the subtypes of gestational diabetes.

Indexed as

Diabetes, GestationalInsulinPlacentaAdultFemaleFetusHumansPregnancyVasodilationInsulinEndothelial functionFetal placental vesselsGestational diabetesSubstance P

Identifiers

PMID39384641
PMCPMC11711144

What Socratic 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 Socratic graph.