The impact of obesity on placental vascular development and function

Maternal obesity is complicating an increasing number of pregnancies globally and is associated with a heightened risk of adverse obstetric and fetal outcomes. The placenta, which mediates maternal-fetal exchange, is postulated to be a key mediator of these outcomes. The development of the extensively branched placental vascular network, driven by spatial and temporal regulation of angiogenic cues, is critical to ensure efficient exchange capacity. In maternal obesity, the placenta exhibits lipotoxicity, inflammation, and a range of cellular stresses, which may impair angiogenic signalling and endothelial metabolism, thereby disrupting vascular development. Understanding the timing and nature of obesity-induced disruptions to placental vascular development is important to improve clinical monitoring, inform the development of targeted interventions to improve fetal outcomes, and reduce obesity-associated pregnancy complications. This review synthesizes the current literature on the impact of maternal obesity on the placental vasculature, considering how changes in vascular architecture, angiogenic factors, and endothelial cell metabolism intersect to lead to dysfunction. Furthermore, we propose a conceptual framework to explain how distinct combinations of placental alterations may underlie the heightened risk of divergent fetal growth outcomes (both pathologically large and small babies) commonly observed in obese pregnancies.