Gestational diabetes & diabetes in pregnancy

Mechanisms of vascular endothelial cell injury triggered by blood glucose changes in gestational diabetes mellitus

Diabetes Obes MetabPublished Mechanistic study

Authors' conclusion

The findings demonstrate that alterations in glucose concentration, particularly the shift from high to low levels, can lead to vascular endothelial cell dysfunction, increase ROS levels, and are associated with the TGF β/SMAD3 signalling pathway. Furthermore, compromised HUVECs can influence the microenvironment via their secretions, potentially jeopardising the health of both the mother and foetus.

Study context

Population
Pregnant women with and without GDM; Human umbilical vein endothelial cells (HUVECs) from six pairs of pregnant women
Participants
67 vs 68
Comparison
GDM vs healthy pregnancy; varying glucose concentrations in HUVECs
  • GDMn = 67
  • Healthyn = 68reference
Methodological detailsclinical data analysis, transcriptomic sequencing, cellular experiments
  • Clinical data analysis
  • Transcriptomic sequencing
  • Cellular experiments

Main finding

As reported in the abstract

  • In GDM, early pregnancy hyperglycemia significantly linked to adverse pregnancy outcomes, even with well-controlled blood glucose
  • Significant alterations in HUVEC gene expression under GDM conditions, enriched in metabolism, inflammation, oxidative stress and diabetes signalling pathway genes
  • Shift in glucose concentration from elevated to reduced levels damages HUVECs, causes dysfunction, elevates ROS and activates TGF-β signalling
  • Injured HUVECs release CTGF via TGF-β signalling, influencing extracellular matrix and surrounding cells

Original publication

Mechanisms of vascular endothelial cell injury triggered by blood glucose changes in gestational diabetes mellitus. Diabetes Obes Metab. Published 13 May 2025. doi:10.1111/dom.16450

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