Rosa Korpershoek

Placental metabolism is essential for maintaining fetal growth and maternal adaptation to pregnancy. Fatty acids are often overlooked as an energy substrate for the placenta. Work from our group and collaborators has shown a capacity for fatty acid oxidation (FAO) in sheep, human and mouse placenta. Moreover, under hypoxic or oxidative stress conditions, as seen in pregnancy complications such as preeclampsia and at high altitude, placental FAO is markedly suppressed. However, fatty acids are crucial for membrane phospholipid, cholesterol, and triglyceride synthesis.

We hypothesise that hypoxia alters mitochondrial oxidative capacity, including FAO, which can cause accumulation of potentially lipotoxic lipid species. Such lipid-induced oxidative and inflammatory stress may contribute to the placental dysfunction characteristics of preeclampsia and fetal growth restriction. My work will therefore aim to determine how hypoxia impacts FAO capacity and lipid homeostasis in the placenta. Further, I aim to clarify whether hypoxia-induced suppression of FAO represents an adaptive or maladaptive response, and how it contributes to placental lipotoxicity and adverse pregnancy outcomes.