Found programs: National Natural Science Foundation of China(Nos.81973596,82004412);Doctoral Start-up Foundation of Henan University of Chinese Medicine(No.RSBSJJ2019-29);Traditional Chinese Medicine Inheritance and Innovation Talent Project(Zhongjing Project) Traditional Chinese Medicine Youth Talent Training Program of Henan Province(YuWei Chinese Medicine [2021],No.16);Special Project of Traditional Chinese Medicine Scientific Research of Henan Province(No.2024ZY3006);Key Research and Development Program of Henan Province (No.241111310900)
Authors：Zhao Qi; Chen Ping; Yang Liping; Sun Jianhua
Keywords：polycystic ovary syndrome; mitochondrial autophagy; ferroptosis; tandem mechanism; granulosa cells;
DOI：10.19405/j.cnki.issn1000-1492.2025.06.025
〔Abstract〕 Polycystic ovarian syndrome(PCOS) is a very common endocrine and reproductive disease. Its etiology and pathogenesis are complex and not yet fully clear. At present, the clinical treatment is mainly symptomatic. Studies have revealed that ferroptosis, as a new form of cell death, may play a key regulatory role in the occurrence and development of PCOS. In addition, there is an increase in autophagy/mitochondrial autophagy in PCOS patients, which may be closely related to the occurrence of ferroptosis. This review summarizes the pathogenesis of mitochondrial autophagy and ferroptosis in PCOS, and analyzes the interrelationship between mitochondrial autophagy and ferroptosis in granulosa cells, in order to provide new insights and potential therapeutic targets for the clinical treatment of PCOS.