Fetal growth restriction (FGR) occurs when the fetus fails to reach its predetermined growth potential and affects approximately 10% of births in Australia. FGR is characterised by placental insufficiency, with FGR placentae being smaller in size and weight than healthy term placentae and comprising of underdeveloped placental villi – the site of exchange between the maternal and fetal systems. These changes are suggested to arise from poor trophoblast function, although the underlying mechanisms remain elusive. Our recent work has established that mitochondria are essential for optimal trophoblast and placental function. Using cryo-electron tomography and array tomography we have mapped the mitochondrial networks of healthy villous trophoblast cells. This work determined a complex withdrawal of mitochondrial mechanisms accompany cellular differentiation to support cell specific functions in the placental villi. Notably, the abundance of mitochondrial dynamics, structural membrane proteins, and electron transport chain proteins determine mitochondrial morphology, cristae curvature, and thereby function. We have shown that many of these mitochondrial mechanisms are dysfunctional in FGR, resulting in a lack the bioenergetic capacity. We propose these changes precede impaired trophoblast cell growth, leading to poor placental development, and in turn failure of the fetus to grow. A hypothesis supported by genome wide association studies (>250,000 individuals), Sanger sequencing (n=13), proteomics (n=12), western blotting (n=7) and qt-PCR (n=19), which identified altered gene expression and protein abundance in FGR. These findings have provided numerous therapeutic targets and pathways we have begun to investigate within a plate based knockdown model of FGR. Using the Incucyte to assess growth, and Xcelligence to measure invasion of trophoblasts through impedance. We have shown that supporting mitochondrial function improves and restores growth and invasion capacity in trophoblasts. Collectively this work provides insights into the importance of mitochondria to cellular and placental function, highlights their complex role in pathology, and assesses the feasibility of restoring mitochondrial function to aid in placental development and improve growth trajectories in FGR.