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本文引用的文献

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Age-dependent integrity of the meiotic spindle assembly checkpoint in females requires Aurora kinase B.在女性中,依赖年龄的减数分裂纺锤体组装检查点的完整性需要 Aurora 激酶 B。
Aging Cell. 2021 Nov;20(11):e13489. doi: 10.1111/acel.13489. Epub 2021 Oct 26.
2
Meiotic Cohesin and Variants Associated With Human Reproductive Aging and Disease.与人类生殖衰老和疾病相关的减数分裂黏连蛋白及其变体
Front Cell Dev Biol. 2021 Aug 2;9:710033. doi: 10.3389/fcell.2021.710033. eCollection 2021.
3
Integrated stress response control of granulosa cell translation and proliferation during normal ovarian follicle development.在正常卵巢卵泡发育过程中,颗粒细胞翻译和增殖的综合应激反应控制。
Mol Hum Reprod. 2021 Aug 7;27(8). doi: 10.1093/molehr/gaab050.
4
Diagnosis and Management of Infertility: A Review.不孕不育的诊断与管理:综述。
JAMA. 2021 Jul 6;326(1):65-76. doi: 10.1001/jama.2021.4788.
5
Human amnion-derived mesenchymal stem cells improved the reproductive function of age-related diminished ovarian reserve in mice through Ampk/FoxO3a signaling pathway.人羊膜间充质干细胞通过 Ampk/FoxO3a 信号通路改善了与年龄相关的卵巢储备减少小鼠的生殖功能。
Stem Cell Res Ther. 2021 Jun 2;12(1):317. doi: 10.1186/s13287-021-02382-x.
6
The Role of Oxidative Stress and Natural Antioxidants in Ovarian Aging.氧化应激与天然抗氧化剂在卵巢衰老中的作用
Front Pharmacol. 2021 Jan 14;11:617843. doi: 10.3389/fphar.2020.617843. eCollection 2020.
7
Delaying Reproductive Aging by Ovarian Tissue Cryopreservation and Transplantation: Is it Prime Time?通过卵巢组织冻存和移植延缓生殖衰老:是否为时过早?
Trends Mol Med. 2021 Aug;27(8):753-761. doi: 10.1016/j.molmed.2021.01.005. Epub 2021 Feb 4.
8
Inhibition of the NLRP3 inflammasome prevents ovarian aging.抑制NLRP3炎性小体可预防卵巢衰老。
Sci Adv. 2021 Jan 1;7(1). doi: 10.1126/sciadv.abc7409. Print 2021 Jan.
9
Evaluation of inflammation and follicle depletion during ovarian ageing in mice.评估小鼠卵巢衰老过程中的炎症和卵泡耗竭。
Sci Rep. 2021 Jan 11;11(1):278. doi: 10.1038/s41598-020-79488-4.
10
DNA Damaged Induced Cell Death in Oocytes.DNA 损伤诱导的卵母细胞细胞死亡。
Molecules. 2020 Dec 3;25(23):5714. doi: 10.3390/molecules25235714.

衰老的卵巢与从胎儿发育中获得的启示。

The Aging Ovary and the Tales Learned Since Fetal Development.

机构信息

Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, Connecticut, USA.

Department of Obstetrics and Gynecology, University of Colorado Denver, Aurora, Colorado, USA.

出版信息

Sex Dev. 2023;17(2-3):156-168. doi: 10.1159/000532072. Epub 2023 Aug 18.

DOI:10.1159/000532072
PMID:37598664
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10841896/
Abstract

BACKGROUND

While the term "aging" implies a process typically associated with later life, the consequences of ovarian aging are evident by the time a woman reaches her forties, and sometimes earlier. This is due to a gradual decline in the quantity and quality of oocytes which occurs over a woman's reproductive lifespan. Indeed, the reproductive potential of the ovary is established even before birth, as the proper formation and assembly of the ovarian germ cell population during fetal life determines the lifetime endowment of oocytes and follicles. In the ovary, sophisticated molecular processes have been identified that regulate the timing of ovarian aging and these are critical to ensuring follicular maintenance.

SUMMARY

The mechanisms thought to contribute to overall aging have been summarized under the term the "hallmarks of aging" and include such processes as DNA damage, mitochondrial dysfunction, telomere attrition, genomic instability, and stem cell exhaustion, among others. Similarly, in the ovary, molecular processes have been identified that regulate the timing of ovarian aging and these are critical to ensuring follicular maintenance. In this review, we outline critical processes involved in ovarian aging, highlight major achievements for treatment of ovarian aging, and discuss ongoing questions and areas of debate.

KEY MESSAGES

Ovarian aging is recognized as what may be a complex process in which age, genetics, environment, and many other factors contribute to the size and depletion of the follicle pool. The putative hallmarks of reproductive aging outlined herein include a diversity of plausible processes contributing to the depletion of the ovarian reserve. More research is needed to clarify if and to what extent these putative regulators do in fact govern follicle and oocyte behavior, and how these signals might be integrated in order to control the overall pattern of ovarian aging.

摘要

背景

虽然“衰老”一词暗示了一个与晚年相关的过程,但女性到四十多岁时,甚至更早,就已经能明显感受到卵巢衰老的后果。这是由于卵母细胞的数量和质量随着女性的生殖寿命逐渐下降所致。事实上,即使在出生前,卵巢的生殖潜能就已经确定了,因为胎儿期卵巢生殖细胞群体的正确形成和组装决定了卵母细胞和卵泡的终生储备。在卵巢中,已经确定了调节卵巢衰老时间的复杂分子过程,这些过程对于确保卵泡的维持至关重要。

总结

被称为“衰老标志”的术语概括了被认为导致整体衰老的机制,包括 DNA 损伤、线粒体功能障碍、端粒磨损、基因组不稳定性和干细胞耗竭等过程。同样,在卵巢中,已经确定了调节卵巢衰老时间的分子过程,这些过程对于确保卵泡的维持至关重要。在这篇综述中,我们概述了卵巢衰老过程中涉及的关键过程,强调了治疗卵巢衰老的主要成就,并讨论了正在进行的问题和争议领域。

关键信息

卵巢衰老被认为是一个复杂的过程,其中年龄、遗传、环境和许多其他因素都会影响卵泡池的大小和耗竭。本文概述的生殖衰老的假定标志包括许多可能导致卵巢储备耗竭的过程。需要进一步的研究来澄清这些假定的调节因子是否以及在何种程度上确实控制了卵泡和卵母细胞的行为,以及这些信号如何整合以控制卵巢衰老的整体模式。