From gut dysbiosis to placental dysfunction in maternal obesity: A common soil for gestational complications

Maternal obesity constitutes a risk factor for gestational complications and adverse pregnancy outcomes. While insulin resistance, metabolic syndrome, and inflammation are recognized contributors, the clinical heterogeneity among these disorders suggests the involvement of systemic, cross-organ interactions. Among these, the gut-placenta axis has become a mechanistic bridge linking maternal metabolism with placental development and fetal health. This review examines the evolution of the gut-placenta axis over the past 50 years and looks forward to its clinical translation in the next 50 years. The obesity-related gut microbiota alterations and their associations with placental dysfunction are summarized. We propose that obesity-induced gut dysbiosis establishes a shared pathophysiological foundation, or “common soil”, characterized by microbial translocation, inflammation at the maternal-fetal interface, and abnormal placental vascularization. From this shared foundation emerge diseases including gestational diabetes mellitus (GDM), preeclampsia (PE), and fetal growth restriction (FGR). Current microbiota-targeted interventions have demonstrated partial metabolic improvements but limited clinical efficacy, highlighting the need for better experimental models, optimal timing, and targeted delivery. Ultimately, targeting this common soil may enable a transition from association to prevention, and transform obesity-related pregnancy complications from adverse outcomes into preventable conditions.