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

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology Vol. 313; no. 4; pp. R395 - R399
• Main Authors: Aljunaidy, Mais M, Morton, Jude S, Cooke, Christy-Lynn M, Davidge, Sandra T
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.10.2017
• Subjects: Animals; Antioxidants; Cardiovascular disease; Cardiovascular diseases; Cardiovascular Diseases - etiology; Cardiovascular Diseases - metabolism; Female; Fetal Development - physiology; Fetal Growth Retardation - metabolism; Fetuses; Humans; Hypoxia; Hypoxia - metabolism; Linkages; Mitochondria; Morbidity; Nanoparticles; Offspring; Oxidative stress; Oxidative Stress - physiology; Placenta; Placenta - metabolism; Placental Insufficiency - metabolism; Pregnancy; cardiovascular disease; hypoxia; placenta; DOHaD; oxidative stress
• ISSN: 0363-6119; 1522-1490
• DOI: 10.1152/ajpregu.00245.2017

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.