As the basic functional unit within mammalian ovaries, each follicle comprises an oocyte surrounded by one or more layers of granulosa cells (GCs). Some follicles are recruited and selected by pituitary gonadotropins to develop towards ovulation. However, more than 99% of the follicles undergo degeneration during growth and development, a phenomenon known as follicular atresia. Inappropriate follicular atresia is responsible for certain reproductive disorders, such as polycystic ovarian syndrome and premature ovarian failure, leading to infertility in women. Traditionally, follicular atresia was thought to occur entirely by GC apoptosis. However, recent literature suggests that nonapoptotic forms of programmed cell death (PCD) such as autophagy may also be involved. Over the past decade, studies have demonstrated that autophagy occurred in GCs and oocytes plays a critical role in determining the developmental fate of ovarian follicles, whether undergo atresia or ovulation, although the underlying mechanisms remains largely undetermined.
The expression of autophagy related genes (Atg) is detectable throughout the ovary. Mice with Atg knockout exhibited fewer germ cells and follicles in the ovary, and become sterile over time. During follicular development, autophagosomes have been observed more frequently in oocytes within pre-antral follicles, while autophagy in antral follicles mainly occurs in the GCs. The induction of autophagy in GCs and oocytes showed both pro-survival and pro-death effects on the follicles. For instance, under hypoxia conditions, the selective degradation of damaged mitochondria in GCs could mitigate the apoptosis and atresia in developing follicles. However, under conditions of extreme stress, such as chemotherapy, excessive autophagy might induce follicular atresia through a combined effect of autophagy and apoptosis. Moreover, autophagy has been reported to initiate or prevent follicular atresia without apoptosis induction in ovarian cells. Therefore, it remains to be determined whether, among the complex functions of autophagy, there are specific subsets of target effectors under different circumstances. These studies might provide novel insights into the mechanism required for developmental fate decision in ovarian follicles.
In this Research Topic, we welcome original research and review articles promoting discussion on all areas relating but not limited to:
• Autophagic signaling involved in follicular development/atresia
• The interaction between autophagy and apoptosis in follicular development/atresia
• The ovarian local factors in the regulation of autophagy during follicular development/atresia
• The cross-regulation of hormones and autophagy on endocrine cell signaling and function in ovarian follicles
• Autophagy in the pathogenesis of ovarian diseases
• Autophagy and oogenesis
As the basic functional unit within mammalian ovaries, each follicle comprises an oocyte surrounded by one or more layers of granulosa cells (GCs). Some follicles are recruited and selected by pituitary gonadotropins to develop towards ovulation. However, more than 99% of the follicles undergo degeneration during growth and development, a phenomenon known as follicular atresia. Inappropriate follicular atresia is responsible for certain reproductive disorders, such as polycystic ovarian syndrome and premature ovarian failure, leading to infertility in women. Traditionally, follicular atresia was thought to occur entirely by GC apoptosis. However, recent literature suggests that nonapoptotic forms of programmed cell death (PCD) such as autophagy may also be involved. Over the past decade, studies have demonstrated that autophagy occurred in GCs and oocytes plays a critical role in determining the developmental fate of ovarian follicles, whether undergo atresia or ovulation, although the underlying mechanisms remains largely undetermined.
The expression of autophagy related genes (Atg) is detectable throughout the ovary. Mice with Atg knockout exhibited fewer germ cells and follicles in the ovary, and become sterile over time. During follicular development, autophagosomes have been observed more frequently in oocytes within pre-antral follicles, while autophagy in antral follicles mainly occurs in the GCs. The induction of autophagy in GCs and oocytes showed both pro-survival and pro-death effects on the follicles. For instance, under hypoxia conditions, the selective degradation of damaged mitochondria in GCs could mitigate the apoptosis and atresia in developing follicles. However, under conditions of extreme stress, such as chemotherapy, excessive autophagy might induce follicular atresia through a combined effect of autophagy and apoptosis. Moreover, autophagy has been reported to initiate or prevent follicular atresia without apoptosis induction in ovarian cells. Therefore, it remains to be determined whether, among the complex functions of autophagy, there are specific subsets of target effectors under different circumstances. These studies might provide novel insights into the mechanism required for developmental fate decision in ovarian follicles.
In this Research Topic, we welcome original research and review articles promoting discussion on all areas relating but not limited to:
• Autophagic signaling involved in follicular development/atresia
• The interaction between autophagy and apoptosis in follicular development/atresia
• The ovarian local factors in the regulation of autophagy during follicular development/atresia
• The cross-regulation of hormones and autophagy on endocrine cell signaling and function in ovarian follicles
• Autophagy in the pathogenesis of ovarian diseases
• Autophagy and oogenesis
