Gene/Protein
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Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Enzyme
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Query: UMLS:C0242706 (
hyperoxia
)
5,219
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
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 O
2
(less than 2-8% O
2
in human; chronic physiological normoxia,
CPN
) throughout pregnancy. O
2
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 O
2
(~21% O
2
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.
...
PMID:Role of oxygen in fetoplacental endothelial responses: hypoxia, physiological normoxia, or hyperoxia? 3226 17
