FERTILITY, IVF AND REPRODUCTIVE GENETICS: Edited by Emre Seli and Juan A. García VelascoMitochondrial function in women with polycystic ovary syndromeCozzolino, Mauroa,b,c; Seli, Emrea,dAuthor Information aDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut, USA bUniversidad Rey Juan Carlos, Madrid, Spain cIVIRMA, IVI Foundation, Valencia, Spain dIVIRMA New Jersey, Basking Ridge, New Jersey, USA Correspondence to Emre Seli, MD, Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, 310 Cedar Street LSOG 304B, New Haven, CT 06520-8063, USA. Tel: +1 203 785 7873; fax: +1 203 785 7819; e-mail: [email protected] Current Opinion in Obstetrics and Gynecology: June 2020 - Volume 32 - Issue 3 - p 205-212 doi: 10.1097/GCO.0000000000000619 Buy Metrics Abstract Purpose of review To provide an overview of mitochondrial functional alterations in women with polycystic ovary syndrome (PCOS). Recent findings Although numerous studies have focused on PCOS, the pathophysiological mechanisms that cause this common disease remain unclear. Mitochondria play a central role in energy production, and mitochondrial dysfunction may underlie several abnormalities observed in women with PCOS. Recent studies associated mtDNA mutations and low mtDNA copy number with PCOS, and set out to characterize the potential protective role of mitochondrial and endoplasmic reticulum unfolded protein responses (UPRmt and UPRer). Summary Mitochondrial dysfunction likely plays a role in the pathogenesis of PCOS by increasing reactive oxygen (ROS) and oxidative stress. This occurs in a metabolic milieu often affected by insulin resistance, which is a common finding in women with PCOS, especially in those who are overweight or obese. Mutations in mtDNA and low mtDNA copy number are found in these patients and may have potential as diagnostic modalities for specific PCOS phenotypes. More recently, UPRer and UPRmt are being investigated as potential cellular rescue mechanisms in PCOS, the failure of which may lead to apoptosis, and contribute to decreased reproductive potential. Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.