Redox imbalance and mitochondrial dysfunction in gestational diabetes mellitus: Implications for maternal health, placental function, and offspring metabolic programming.

Mitochondrial dysfunction and redox imbalance are increasingly recognised as essential factors in the pathophysiology of gestational diabetes mellitus (GDM). Impaired oxidative phosphorylation in the placenta, increased production of reactive oxygen species (ROS), and insufficient antioxidant protection impair bioenergetics and affect maternal-foetal nutrient exchange. Such changes promote excessive foetal growth and metabolic programming while predisposing mothers to future type 2 diabetes. Current research indicates alterations in mitochondrial dynamics and mitophagy as additional risk factors for placental disease. The placenta is not only a passive recipient of maternal hyperglycaemia; it actively participates in metabolic signalling at the maternal-foetal interface. This structure identifies placental mitochondria as potential therapeutic targets. Preclinical studies on mitochondrial antioxidants (SS-31, MitoQ), uncoupling factors, and biogenesis-supporting substances have shown great potential in restoring mitochondrial integrity and reducing oxidative stress. However, there is still no clinical confirmation of their effectiveness during pregnancy. A comprehensive understanding of mitochondrial redox processes during gestational diabetes offers unique potential for improving pregnancy outcomes and may contribute to reducing the intergenerational inheritance of metabolic diseases.