Polycystic ovary syndrome(PCOS)affects female fertility through a variety of complex mechanisms,such as insulin resistance(IR),oxidative stress,chronic inflammation,and subsequent hyperandrogenemia,adipokine secretion disor-der and other factors,changing the external environment for the survival of granular cells.When granulosa cells are stimulated by these external factors,the proportion of anti-apoptotic and pro-apoptotic members in the B-cell lymphoma 2(Bcl-2)family is disproportionally affected,and the intracellular apoptosis pathway is activated,mainly mediated by the mitochondrial pathway.By increasing the permeability of the mitochondrial outer membrane,the mitochondria promote the release of a va-riety of pro-apoptotic proteins such as cytochrome c(Cyt c).Entering the cytoplasm,Cyt c then forms apoptotic corpuscles,which cascade activation of the caspase family and apoptosis of granulosa cells.Once granulosa cell apoptosis occurs,the folli-cles in PCOS patients lose their biological function and the regulation between the cells in the follicle is unbalanced,which pro-motes the apoptosis of oocytes and follicular membrane cells,and eventually leads to the atrexia of follicles.In this paper,we reviewed a large number of relevant literatures to explore the relationship between granulosa cell apoptosis and follicular atresia in PCOS patients and its mechanism.
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