Unraveling mitochondrial dysfunction in polycystic ovary syndrome: Pathophysiological insights

Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder that affects women of reproductive age. It is characterized by ovulatory dysfunction, excessive levels of androgens, and the presence of multiple cysts in the ovaries. Although the exact cause of PCOS remains uncertain, recent studies have identified mitochondrial dysfunction as a key contributing factor. Mitochondria, often described as the energy centers of the cell, are essential for producing ATP, generating reactive oxygen species (ROS), and regulating cell death pathways. A growing body of evidence shows that mitochondrial dysfunction occurs in the ovaries, skeletal muscle, and adipose tissue of individuals with PCOS. This dysfunction may play a central role in the development of the disorder by increasing oxidative stress and chronic inflammation, worsening insulin resistance, and interfering with oocyte growth and quality. This review summarizes recent progress in understanding how mitochondrial dysfunction contributes to the underlying biology of PCOS. It also explores emerging treatment strategies that aim to restore mitochondrial health, such as the use of antioxidants, therapies that specifically target mitochondria, and emerging mitochondrial replacement technologies. These approaches hold promise for reducing the symptoms and long-term complications associated with PCOS.