Purpose

Reproductive decline due to parental age has become a major barrier to fertility as couples have delayed having offspring into their thirties and forties. Advanced parental age is also associated with increased incidence of neurological and cardiovascular disease in offspring. Thus, elucidating the etiology of reproductive decline is of clinical importance.

Methods

Deciphering the underlying processes that drive reproductive decline is particularly challenging in women in whom a discrete oocyte pool is established during embryogenesis and may remain dormant for tens of years. Instead, our understanding of the processes that drive reproductive senescence has emerged from studies in model organisms, both vertebrate and invertebrate, that are the focus of this literature review.

Conclusions

Studies of reproductive aging in model organisms not only have revealed the detrimental cellular changes that occur with age but also are helping identify major regulator proteins controlling them. Here, we discuss what we have learned from model organisms with respect to the molecular mechanisms that maintain both genome integrity and oocyte quality.

中文翻译：

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生殖衰老的分子基础：来自模式生物的见解

目的

由于父母年龄导致的生育能力下降已成为生育的主要障碍，因为夫妻将后代推迟到三四十岁。父母年龄高也与后代神经系统和心血管疾病的发病率增加有关。因此，阐明生殖衰退的病因具有临床意义。

方法

对于在胚胎发育过程中建立离散卵母细胞池并且可能保持休眠数十年的女性来说，破译导致生殖衰退的潜在过程尤其具有挑战性。相反，我们对驱动生殖衰老的过程的理解来自对模式生物（包括脊椎动物和无脊椎动物）的研究，这是本文献综述的重点。

结论

对模式生物生殖衰老的研究不仅揭示了随着年龄增长而发生的有害细胞变化，而且有助于识别控制它们的主要调节蛋白。在这里，我们讨论了我们从模式生物中学到的关于维持基因组完整性和卵母细胞质量的分子机制。