The mechanism of autophagy in granulosa cells during the follicular development.

During follicular development, granulosa cell autophagy is dynamically involved in follicular growth, atresia, estrogen and progesterone synthesis, luteinization, and luteal regression. Granulosa cell autophagy is regulated by gonadotropins, estrogen, progesterone, oxidative stress, and multiple signaling pathways. Conversely, granulosa cell autophagy can also influence estrogen and progesterone synthesis by regulating lipid metabolism, mitochondrial quality control, and granulosa cell viability.However, the biological effects of autophagy are highly context-dependent. Moderate autophagy is an important mechanism for maintaining granulosa cell homeostasis and promoting follicular development, whereas excessive autophagy or impaired autophagic flux may lead to granulosa cell dysfunction, increased apoptosis, follicular atresia, and reproductive endocrine disorders. Dysregulated granulosa cell autophagy has been closely associated with ovulatory disorders such as polycystic ovary syndrome and premature ovarian insufficiency. Therefore, promoting follicular development through the regulation of autophagy may provide an important therapeutic entry point for ovulatory disorders. This review summarizes the roles and underlying mechanisms of granulosa cell autophagy in follicular development, follicular atresia, hormonal regulation, and ovulatory disorders, and proposes that maintaining autophagic homeostasis may represent a potential strategy for promoting follicular development and improving female reproductive health.