The Role of Mitochondrial Dysfunction and Oxidative Stress in Women’s Reproductive Disorders: Implications for Polycystic Ovary Syndrome and Preeclampsia

Abstract

Despite decades of research, the pathophysiology of preeclampsia (PE) and polycystic ovary syndrome (PCOS) remains poorly understood. Notably, no new FDA-approved treatments for PE have emerged in over 50 years. PCOS, a common endocrine disorder, increases a woman’s risk of developing PE. Both conditions share overlapping mechanisms, including insulin resistance, chronic inflammation, endothelial dysfunction, and oxidative stress. While physiological levels of reactive oxygen species (ROS) are essential for reproduction, excess ROS contributes to cellular and mitochondrial damage. This review will assess current evidence linking oxidative stress and mitochondrial dysfunction to the development of PCOS and PE, explore their shared mechanisms, and evaluate emerging therapeutic interventions. Ultimately, a comprehensive understanding of these shared mechanisms may inform strategies for early prediction, prevention, and the treatment of PE and PCOS.