Adenosine kinase and cardiovascular fetal programming in gestational diabetes mellitus

Luis Silva, Torsten Plösch, Fernando Toledo, Marijke M Faas*, Luis Sobrevia*

*Corresponding author for this work

Research output: Contribution to journalReview articleAcademicpeer-review

6 Citations (Scopus)
4 Downloads (Pure)

Abstract

Gestational diabetes mellitus (GDM) is a detrimental condition for human pregnancy associated with endothelial dysfunction and endothelial inflammation in the fetoplacental vasculature and leads to increased cardio-metabolic risk in the offspring. In the fetoplacental vasculature, GDM is associated with altered adenosine metabolism. Adenosine is an important vasoactive molecule and is an intermediary and final product of transmethylation reactions in the cell. Adenosine kinase is the major regulator of adenosine levels. Disruption of this enzyme is associated with alterations in methylation-dependent gene expression regulation mechanisms, which are associated with the fetal programming phenomenon. Here we propose that cellular and molecular alterations associated with GDM can dysregulate adenosine kinase leading to fetal programming in the fetoplacental vasculature. This can contribute to the cardio-metabolic long-term consequences observed in offspring after exposure to GDM.

Original languageEnglish
Article number165397
Number of pages11
JournalBiochimica et biophysica acta-Molecular basis of disease
Volume1866
Issue number2
Early online date27-Jan-2019
DOIs
Publication statusPublished - 1-Feb-2020

Keywords

  • Adenosine kinase
  • Fetal programming
  • Placenta
  • Endothelium
  • Gestational diabetes
  • VEIN ENDOTHELIAL-CELLS
  • DNA METHYLATION
  • NITRIC-OXIDE
  • S-ADENOSYLHOMOCYSTEINE
  • EPIGENETIC REGULATION
  • UMBILICAL-CORD
  • INTRAUTERINE EXPOSURE
  • NUCLEOSIDE TRANSPORT
  • INSULIN-RESISTANCE
  • HUMAN PLACENTA

Cite this