Division of Reproductive Endocrinology and Infertility, Department of Obstetrics, Gynecology, & Reproductive Sciences, Yale School of Medicine, 333 Cedar Street FMB, 329F, New Haven, CT, 06520-8023, USA.
Adv Exp Med Biol. 2013;761:7-18. doi: 10.1007/978-1-4614-8214-7_2.
Mechanisms that control the survival of oocytes and, by extension, the duration of ovarian function have been identified. However, it is still not clear whether oocyte "quality" is related to survival, nor is the role of the granulosa cells of follicles in follicle survival entirely understood. Here, we consider oocyte-intrinsic and oocyte-extrinsic mechanisms of oocyte loss and argue that developing a better understanding of such physiological events is needed to protect fertility, fecundity, and ovarian function in women.The duration that ovaries function is, as is intuitive, controlled by the number of remaining oocytes within follicles. Once the number of follicles drops beneath a threshold number, ovarian function ceases. Thus, understanding mechanisms that control oocyte survival is paramount as we consider strategies to protect or prolong ovarian function in women. It is often assumed that physiological oocyte survival is entirely controlled by "oocyte- intrinsic" factors, such as poor genetic quality or accumulated damage to the oocyte itself. Oocytes that have poor genetic quality due to development or accumulated damage would then die sooner than those of higher "quality." Indeed, new data suggest that oocyte-intrinsic genetic quality as determined by the ability to repair double-stranded DNA breaks is a significant contributor to oocyte survival and the duration of ovarian function. However, the nature of the follicle, where the oocyte and surrounding granulosa cells exist in intimate contact and rely upon each other for survival signals and metabolic function, makes it unlikely that oocyte-intrinsic factors entirely control oocyte survival. We and others are assessing the role of adjacent somatic (granulosa) cells in follicle survival, determining the relative importance of "oocyte-extrinsic" factors.
控制卵母细胞存活的机制已被确定，并且可以扩展到卵巢功能的持续时间。然而，目前尚不清楚卵母细胞“质量”是否与存活有关，也不完全了解卵泡颗粒细胞在卵泡存活中的作用。在这里，我们考虑卵母细胞内在和卵母细胞外在的卵母细胞丢失机制，并认为需要更好地理解这些生理事件，以保护女性的生育能力、生育力和卵巢功能。
卵巢功能的持续时间直观地受到卵泡内剩余卵母细胞数量的控制。一旦卵泡数量降至阈值以下，卵巢功能就会停止。因此，了解控制卵母细胞存活的机制对于我们考虑保护或延长女性卵巢功能的策略至关重要。
通常认为，生理卵母细胞的存活完全由“卵母细胞内在”因素控制，例如遗传质量差或卵母细胞本身积累的损伤。由于发育或积累的损伤而遗传质量差的卵母细胞会比质量较高的卵母细胞更早死亡。事实上，新数据表明，卵母细胞内在的遗传质量，如修复双链 DNA 断裂的能力，是卵母细胞存活和卵巢功能持续时间的重要因素。
然而，卵泡的性质使得卵母细胞内在因素不可能完全控制卵母细胞的存活。我们和其他人正在评估相邻的体细胞（颗粒细胞）在卵泡存活中的作用，确定“卵母细胞外在”因素的相对重要性。
