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Factors influencing establishment of the ovarian reserve and their effects on fertility

机译：影响卵巢保护区建立的因素及其对生育力的影响

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A reserve of primordial follicles is set up in the ovaries of fetuses or neonates, depending on the species, and serves as the source of developing follicles throughout the reproductive lifespan. This review focuses on the cellular and molecular mechanisms currently known to control the establishment of this reserve, and their regulation by environmental factors. Most mutations in genes controlling germ cell proliferation and survival, meiosis or follicle assembly lead to the absence of primordial follicles or a sharp reduction in their number, incompatible with fertility in adults. Inadequate maternal nutrition affects the cellular metabolism, increases the oxidative stress and delays follicle formation in fetal ovaries. Despite the existence of compensation mechanisms of some developmental processes, the early-life nutritional environment imprints the long-term ability of follicles to enter growth and develop in adult ovaries. However, maternal undernutrition, overfeeding or high-fat diet during the establishment of the ovarian reserve does not seem to affect the fertility of the female offspring, unless their metabolism or neuroendocrine status is altered. Exposure of fetal or neonatal ovaries to excess steroids inhibits or stimulates follicle formation in a complex manner depending on the nature of the steroid, the dose and the animal species. Estrogens can control follicle formation through intra-ovarian mechanisms involving members of the TGF-beta family such as activin and BMP2. Early-life exposure to synthetic estrogens or environmental pollutants with estrogen-like activity impairs meiotic progression and follicle assembly, and affects long-term primordial follicle activation in adult ovaries. The effects of compounds with estrogen-like activity on the ovarian reserve can be transmitted to several generations through the female germline. Further investigations are needed to establish the early-life effects of the environmental factors on the female reproductive lifespan and decipher the mechanisms of their epigenetic effects on the size and quality of the ovarian reserve.
机译：在胎儿或新生儿的卵巢中，依物种而定，形成了原始卵泡储备，并在整个生殖寿命中作为发育中的卵泡来源。这项审查侧重于目前已知控制该保护区的建立的细胞和分子机制，以及它们受环境因素的调节。控制生殖细胞增殖和存活，减数分裂或卵泡组装的基因中的大多数突变会导致原始卵泡的缺乏或数量的急剧减少，这与成年人的生育能力不相容。孕妇营养不足会影响细胞代谢，增加氧化应激并延迟胎儿卵巢中的卵泡形成。尽管存在某些发育过程的补偿机制，但生命早期的营养环境仍使卵泡在成年卵巢中具有生长发育的长期能力。但是，建立卵巢储备期间的孕产妇营养不足，过度喂养或高脂饮食似乎不会影响雌性后代的生育能力，除非其代谢或神经内分泌状态发生改变。胎儿或新生儿卵巢暴露于过量的类固醇会以类固醇的性质，剂量和动物种类的复杂方式抑制或刺激卵泡形成。雌激素可通过涉及TGF-β家族成员（例如激活素和BMP2）的卵巢内机制控制卵泡形成。生命早期接触合成雌激素或具有雌激素样活性的环境污染物会损害减数分裂进程和卵泡组装，并影响成年卵巢的长期原始卵泡活化。具有雌激素样活性的化合物对卵巢储备的影响可以通过雌性种系传给几代人。需要进一步的研究来确定环境因素对女性生殖寿命的早期影响，并解释其表观遗传影响卵巢储备的大小和质量的机制。

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