Linking Oxidative Stress to Placental Dysfunction: The Key Role of Mitochondria in Trophoblast Function - PubMed
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- #oxidative stress
- #placental dysfunction
- #mitochondria
- Oxidative stress (OS) is a critical regulator of placental development.
- Excessive reactive oxygen species (ROS) disrupt molecular and cellular pathways essential for normal placentation.
- OS impairs mitochondrial function in trophoblasts, leading to increased mitochondrial ROS generation and activation of apoptotic signaling.
- Mitochondrial disturbances are associated with reduced trophoblast proliferation, migration, and invasion.
- OS also dysregulates angiogenic balance and alters mitophagy.
- Redox-sensitive pathways such as CYP1A1 and KLF9 are involved in these processes.
- Extracellular release of mitochondrial DNA is linked to reduced cell viability and increased necrotic cell death.
- OS interferes with key trophoblast-dependent developmental processes, contributing to placental dysfunction in conditions like preeclampsia (PE) and intrauterine growth restriction (IUGR).
- Understanding these pathways may lead to targeted therapeutic strategies to improve pregnancy outcomes.