Role of oxygen in fetoplacental endothelial responses: hypoxia, physiological normoxia, or hyperoxia?
Year: 2020
Type: review
Abstract: During pregnancy, placental vascular growth, which is essential for supporting the rapidly growing fetus, is associated with marked elevations in blood flow. These vascular changes take place under chronic physiological low O2 (less than 2–8% O2 in human; chronic physiological normoxia, CPN) throughout pregnancy. O2 level below CPN pertinent to the placenta results in placental hypoxia. Such hypoxia can cause severe endothelial dysfunction, which is associated with adverse pregnancy outcomes (e.g., preeclampsia) and high risk of adult-onset cardiovascular diseases in children born to these pregnancy complications. However, our current knowledge about the mechanisms underlying fetoplacental endothelial function is derived primarily from cell models established under atmospheric O2 (~21% O2 at sea level, hyperoxia). Recent evidence has shown that fetoplacental endothelial cells cultured under CPN have distinct gene expression profiles and cellular responses compared with cells cultured under chronic hyperoxia. These data indicate the critical roles of CPN in programming fetal endothelial function and prompt us to re-examine the mechanisms governing fetoplacental endothelial function under CPN. Better understanding these mechanisms will facilitate us to develop preventive and therapeutic strategies for endothelial dysfunction-associated diseases (e.g., preeclampsia). This review will provide a brief summary on the impacts of CPN on endothelial function and its underlying mechanisms with a focus on fetoplacental endothelial cells.
Authors: Chi Zhou, Qing-yun Zou, Yi-zhou Jiang, Jing Zheng
Language: English
Subfield: Obstetrics and Gynecology
Field: Medicine
Domain: Health Sciences
Open Access status: green
Awards: Preeclampsia dysregulates fetal endothelial responses to growth factors and cytokines, Preeclampsia-Induced Fetal Endothelial Dysfunction in Obese Pregnancy: Novel roles of miR192-5p, Importance of Endothelial Cell-Cell Communication at the Maternal Fetal Interface, Roles of Novel preeclampsia-associated miR-29 in human endothelial functions, University of Wisconsin Institute for Clinical and Translational Research
OpenAlex ID: W3014691838