Prenatal hypoxia and placental oxidative stress: linkages to developmental origins of cardiovascular disease

Am J Physiol Regul Integr Comp Physiol. 2017 Oct 1;313(4):R395-R399. doi: 10.1152/ajpregu.00245.2017. Epub 2017 Aug 9.

Abstract

Intrauterine growth restriction (IUGR, a pregnancy complication where the fetus does not reach its genetic growth potential) is a leading cause of fetal morbidity and mortality with a significant impact on population health. IUGR is associated with gestational hypoxia; which can lead to placental oxidative stress and fetal programming of cardiovascular disease. Mitochondria are a major source of placental oxidative stress and may provide a therapeutic target to mitigate the detrimental effects of placental oxidative stress on pregnancy outcomes. A nanoparticle-mediated delivery of a mitochondrial antioxidant to the placenta is a potential novel approach that may avoid unwanted off-target effects on the developing offspring.

Keywords: DOHaD; cardiovascular disease; hypoxia; oxidative stress; placenta.

Publication types

  • Review

MeSH terms

  • Animals
  • Cardiovascular Diseases / etiology*
  • Cardiovascular Diseases / metabolism
  • Female
  • Fetal Development / physiology
  • Fetal Growth Retardation / metabolism*
  • Humans
  • Hypoxia / metabolism*
  • Oxidative Stress / physiology*
  • Placenta / metabolism*
  • Placental Insufficiency / metabolism*
  • Pregnancy