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Biochimie. 2018 Dec 31. pii: S0300-9084(18)30361-4. doi: 10.1016/j.biochi.2018.12.016. [Epub ahead of print]

The relationship between the placental serotonin pathway and fetal growth restriction.

Author information

1
Department of Obstetrics and Gynaecology, Monash University, Australia; The Ritchie Centre, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
2
RMIT University, Bundoora, Victoria, Australia.
3
Department of Maternal-Fetal Medicine, Pregnancy Research Centre, Royal Women's Hospital, Parkville, Victoria, Australia.
4
Department of Medicine, School of Clinical Sciences, Clayton, Victoria, Australia.
5
The Ritchie Centre, Hudson Institute of Medical Research, Clayton, Victoria, Australia; Department of Maternal-Fetal Medicine, Pregnancy Research Centre, Royal Women's Hospital, Parkville, Victoria, Australia; Department of Medicine, School of Clinical Sciences, Clayton, Victoria, Australia; Department of Obstetrics and Gynaecology, University of Melbourne, Royal Women's Hospital, Parkville, Victoria, Australia. Electronic address: padma.murthi@monash.edu.

Abstract

Fetal growth restriction (FGR) is a complex disorder of human pregnancy that leads to poor health outcomes in offspring. These range from immediate risks such as perinatal morbidity and stillbirths, to long-term complications including severe neurodevelopmental problems. Despite its relatively high global prevalence, the aetiology of FGR and its complications is not currently well understood. We now know that serotonin (5-HT) is synthesised in the placenta and is crucial for early fetal forebrain development in mice. However, the contribution of a disrupted placental 5-HT synthetic pathway to the pathophysiology of placental insufficiency in FGR and its significant fetal neurodevelopmental complications are unclear.

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