Potential Roles of mtDNA Mutations in PCOS-IR: A Review

Abstract

Xiao-Chao Dong,1 Chang Liu,1 Guang-Chao Zhuo,2 Yu Ding2 1Department of Gynecology and Obstetrics, Hangzhou First People’s Hospital, Zhejiang University School of Medicine, Hangzhou, People’s Republic of China; 2Central Laboratory, Hangzhou First People’s Hospital, Zhejiang University School of Medicine, Hangzhou, People’s Republic of ChinaCorrespondence: Yu Ding, Central Laboratory, Hangzhou First People’s Hospital, Zhejiang University School of Medicine, 261 Huansha Road, Hangzhou, People’s Republic of China, Tel/Fax [phone], Email [email protected]: Polycystic ovary syndrome (PCOS) is the most common heterogeneous endocrine disease that affecting females in reproductive age. Insulin resistance (IR), an important molecular basis for PCOS, accounts for at least 75% of women carrying this syndrome. Although there have been many studies on PCOS-IR, the detailed mechanisms are not fully understood. As essential hub for energy generation, mitochondria are critical to insulin secretion and normal function, whereas mutations in mitochondrial DNA (mtDNA) result in mitochondrial dysfunctions contributing to the pathophysiology of PCOS-IR via the regulation of balance of oxidative stress (OS), energy deficiency, or hormone metabolism. In the current review, we summarize the clinical and molecular features of PCOS-IR and discuss molecular mechanisms related to mtDNA mutations.Keywords: PCOS-IR, mitochondrial dysfunction, mtDNA mutations

Keywords

• pcos-ir
• mitochondrial dysfunction
• mtdna mutations