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 Inherit- ance and Innovation Talent Project ( Zhongjing Project ) Traditional Chinese Medicine Youth Talent Training Pro- gram of Henan Province (YuWei Chinese Medicine [2021] , No . 16) ; Special Project of Traditional Chinese Med- icine Scientific Research of Henan Province ( No . 2024ZY3006 ) ; Key Research and Development Program of Henan Province (No . 241111310900) .
Authors：Zhao Qi 1 , Chen Ping1 , Yang Liping2 , Sun Jianhua1 , 3
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 pa- tients , 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 autoph- agy and ferroptosis in granulosa cells , in order to provide new insights and potential therapeutic targets for the clini- cal treatment of PCOS .