Fetal growth restriction (FGR, babies <3rd growth centile) is a significant clinical issue with no effective treatment other than preterm delivery. The pathophysiology of FGR is established in early pregnancy, but is clinically silent until at least mid-gestation, making this disorder particularly challenging to predict or treat. Indeed, over half of FGR cases remain undetected prior to delivery, and this is a key reason that FGR is the largest risk factor for stillbirth. At its core, FGR results from poor placental exchange function due to a heterogenous combination of factors including impaired trophoblast growth and function, reduced placental villous and vascular branching, and inadequate remodelling of the uterine vasculature. In turn, all these factors combine to impact both the haemodynamics of blood flow in the intervillous space and the resulting placental capacity to transfer nutrients and oxygen to the fetus. In line with the heterogenous pathophysiology of FGR, A/Prof James’ team takes a wide approach to better understand the dynamic events that lead to this disorder across pregnancy, combining stem cell and primary tissue models, in vivo and ex vivo imaging, and in silico tools to integrate physiology across multiple scales and better understand the relationships between distinct pathological components. This talk will cover a spectrum of work focused on understanding the pathophysiology of FGR from the cell to the system level, with a view to improving our ability to better predict, detect, and treat this disorder in the future.