Format

Send to

Choose Destination
Biomed Res Int. 2015;2015:814543. doi: 10.1155/2015/814543. Epub 2015 Jan 29.

Angiogenesis in the placenta: the role of reactive oxygen species signaling.

Author information

1
Department of Pediatrics, McMaster University, Hamilton, ON, Canada L8N 3Z5 ; The Graduate Program in Medical Sciences, McMaster University, 1200 Main Street W., Hamilton, ON, Canada L8N 3Z5.
2
Department of Obstetrics and Gynecology, McMaster University, Hamilton, ON, Canada L8N 3Z5.
3
Department of Pediatrics, McMaster University, Hamilton, ON, Canada L8N 3Z5.
4
The Graduate Program in Medical Sciences, McMaster University, 1200 Main Street W., Hamilton, ON, Canada L8N 3Z5.

Abstract

Proper placental development and function are central to the health of both the mother and the fetus during pregnancy. A critical component of healthy placental function is the proper development of its vascular network. Poor vascularization of the placenta can lead to fetal growth restriction, preeclampsia, and in some cases fetal death. Therefore, understanding the mechanisms by which uterine stressors influence the development of the placental vasculature and contribute to placental dysfunction is of central importance to ensuring a healthy pregnancy. In this review we discuss how oxidative stress observed in maternal smoking, maternal obesity, and preeclampsia has been associated with aberrant angiogenesis and placental dysfunction resulting in adverse pregnancy outcomes. We also highlight that oxidative stress can influence the expression of a number of transcription factors important in mediating angiogenesis. Therefore, understanding how oxidative stress affects redox-sensitive transcription factors within the placenta may elucidate potential therapeutic targets for correcting abnormal placental angiogenesis and function.

PMID:
25705690
PMCID:
PMC4325211
DOI:
10.1155/2015/814543
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Hindawi Limited Icon for PubMed Central
Loading ...
Support Center