Research progress on the effect of mitochondrial and endoplasmic reticulum stress caused by hypoxia during pregnancy on preeclampsia and intrauterine growth restriction.
- Author:
Hui-Fang LIU
1
;
Ri-Li GE
1
;
Ta-Na WUREN
1
Author Information
1. Key Laboratory of Plateau Medicine of Ministry of Education, Plateau Medicine Research Center, Qinghai University, Xining 810001, China.
- Publication Type:Journal Article
- MeSH:
Pregnancy;
Female;
Humans;
Placenta;
Fetal Growth Retardation/etiology*;
Pre-Eclampsia/pathology*;
Reactive Oxygen Species;
Hypoxia/pathology*;
Pregnancy Complications/pathology*;
Endoplasmic Reticulum Stress
- From:
Acta Physiologica Sinica
2023;75(5):714-726
- CountryChina
- Language:Chinese
-
Abstract:
Preeclampsia and intrauterine growth restriction (IUGR) of the fetus are the two most common pregnancy complications worldwide, affecting 5%-10% of pregnant women. Preeclampsia is associated with significantly increased maternal and fetal morbidity and mortality. Hypoxia-induced uteroplacental dysfunction is now recognized as a key pathological factor in preeclampsia and IUGR. Reduced oxygen supply (hypoxia) disrupts mitochondrial and endoplasmic reticulum (ER) function. Hypoxia has been shown to alter mitochondrial reactive oxygen species (ROS) homeostasis and induce ER stress. Hypoxia during pregnancy is associated with excessive production of ROS in the placenta, leading to oxidative stress. Oxidative stress occurs in a number of human diseases, including high blood pressure during pregnancy. Studies have shown that uterine placental tissue/cells in preeclampsia and IUGR show high levels of oxidative stress, which plays an important role in the pathogenesis of both the complications. This review summarizes the role of hypoxia-induced mitochondrial oxidative stress and ER stress in the pathogenesis of preeclampsia/IUGR and discusses the potential therapeutic strategies targeting oxidative stress to treat both the pregnancy complications.
