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Fetoplacental endothelial dysfunction in gestational diabetes mellitus and maternal obesity: A potential threat for

Mariana S Diniz1, Ursula Hiden2, Inês Falcão-Pires3

  • 1CNC - Center for Neuroscience and Cell Biology, CIBB - Centre for Innovative Biomedicine and Biotechnology, University of Coimbra, Coimbra, Portugal; Ph.D. Programme in Experimental Biology and Biomedicine (PDBEB), Institute for Interdisciplinary Research (IIIUC), University of Coimbra, Coimbra, Portugal; Cellular and Molecular Physiology Laboratory (CMPL), Department of Obstetrics, Division of Obstetrics and Gynaecology, School of Medicine, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago 8330024, Chile.

Biochimica Et Biophysica Acta. Molecular Basis of Disease
|August 4, 2023
PubMed

Insights

Gestational diabetes mellitus (GDM) and maternal obesity (MO) can cause fetoplacental endothelial dysfunction, increasing offspring cardiovascular disease risk. Research highlights nitric oxide and L-arginine pathways as key targets.

Area of Science:

  • Obstetrics and Gynecology
  • Cardiovascular Research
  • Developmental Biology

Background:

  • Gestational diabetes mellitus (GDM) and maternal obesity (MO) are linked to adverse fetal outcomes and later-life cardiovascular disease.
  • These conditions may program offspring for disease through mechanisms involving the fetoplacental unit.
  • Fetoplacental endothelial dysfunction is a critical factor in this programming.

Purpose of the Study:

  • To review the role of fetoplacental endothelial dysfunction in offspring cardiovascular disease risk in GDM and MO pregnancies.
  • To examine the impact of maternal health conditions on fetoplacental vascular function and fetal development.
  • To identify key molecular pathways involved in fetoplacental vascular dysfunction.

Main Methods:

  • Literature review focusing on GDM, MO, and fetoplacental endothelial dysfunction.
  • Analysis of studies investigating vascular development and signaling pathways in affected pregnancies.
  • Synthesis of current knowledge on nitric oxide and hydrogen sulfide roles.

Main Results:

  • Maternal health conditions contribute to fetoplacental endothelial dysfunction, impairing fetal cardiovascular development.
  • Nitric oxide and hydrogen sulfide are implicated in mediating fetoplacental vascular dysfunction.
  • The L-Arginine-Nitric Oxide and Adenosine-L-Arginine-Nitric Oxide (ALANO) pathways are identified as crucial targets.

Conclusions:

  • Fetoplacental endothelial dysfunction is a significant mechanism linking maternal GDM/MO to offspring cardiovascular disease.
  • Targeting L-arginine-nitric oxide signaling pathways may offer therapeutic strategies.
  • Further research is needed to address existing knowledge gaps in this field.

Keywords:
Adenosine receptorsCardiac functionEndothelial dysfunctionFetal developmentGestational diabesityMetabolic syndromeNitric oxide

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