Abstract: Autophagy is a degradation pathway in cells. Autophagy at the normal level can remove harmful substances and the damaged organelles to maintain the normal function of cells.  Macroautophagy is the most common form of autophagy. For example, mitochondrial autophagy selectively degrades the dysfunctional mitochondria. Abnormal activation of autophagy is related to the oxidative stress damage of cells. Classical pathways that regulate autophagy include PI3K/AKT-mTOR, AMPK, SIRT1, etc. Studies have confirmed that autophagy of ovarian granulosa cell and oocyte plays an important role in regulating follicular development such as the establishment of primordia follicle pool, follicular recruitment and atresia. Diseases such as polycystic ovary syndrome (PCOS) and primary ovarian insufficiency (POI) are often accompanied by follicular development and atresia dysfunction, resulting in the decreased egg quantity and quality and the decreased female fertility. Autophagy may be involved in the pathophysiological processes of ovarian aging, PCOS and POI. In this paper, autophagy of granulosa cell and oocyte, and its mechanism, as well as autophagy′s involvement in the development and progression of abnormal follicular development and atresia, were reviewed.

Key words: Autophagy；, Oocytes；, Granulosa cells；, Oxidative stress；, Female urogenital diseases