Review
Version 1
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Paradoxes: Cholesterol and Hypoxia in Preeclampsia
Version 1
: Received: 30 April 2024 / Approved: 1 May 2024 / Online: 1 May 2024 (08:09:17 CEST)
How to cite: Hart, N. R. Paradoxes: Cholesterol and Hypoxia in Preeclampsia. Preprints 2024, 2024050063. https://doi.org/10.20944/preprints202405.0063.v1 Hart, N. R. Paradoxes: Cholesterol and Hypoxia in Preeclampsia. Preprints 2024, 2024050063. https://doi.org/10.20944/preprints202405.0063.v1
Abstract
Preeclampsia, a hypertensive disease of pregnancy of unknown etiology, is intensely studied as a model of cardiovascular (CVD) disease not only due to multiple shared pathologic elements, but also because changes that develop over decades in CVD disease appear and resolve within days in preeclampsia. Those affected by preeclampsia and their offspring experience increased lifetime risks of CVD. At the systemic level, preeclampsia is characterized by increased cellular, membrane, and blood levels of cholesterol, however, cholesterol dependent signaling such as canonical Wnt/βcatenin, Hedgehog, and endothelial nitric oxide synthase is downregulated indicating a cholesterol deficit with upregulation of cholesterol synthesis and efflux. Hypoxia related signaling in preeclampsia also appears paradoxical with increased Hypoxia Inducible Factors (HIF) in the placenta but measurably increased oxygen in maternal blood in placental villous spaces. This review addresses the molecular mechanisms by which excessive systemic cholesterol and deficient cholesterol dependent signaling may arise from the effects of dietary lipid variance causing the cellular hypoxia which characterizes preeclampsia.
Keywords
preeclampsia; hypoxia inducible factors; cholesterol; dietary lipids; Hedgehog (Hh); Wnt/βcatenin; membrane biophysics; endothelial nitric oxide synthase; dyslipidemia; oxidative stress
Subject
Biology and Life Sciences, Other
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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