Quesada-Candela Cristina, Loose Julia, Ghazi Arjumand, Yanowitz Judith L
Magee-Womens Research Institute, Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Pittsburgh School of Medicine, 204 Craft Avenue, Pittsburgh, PA, 15213, USA.
Departments of Pediatrics, Developmental Biology and Cell Biology and Physiology, John G. Rangos Sr. Research Center, University of Pittsburgh School of Medicine, Room 7129, One Children's Hospital Drive, 4401 Penn Avenue, Pittsburgh, PA, 15224, USA.
J Assist Reprod Genet. 2021 Jan;38(1):17-32. doi: 10.1007/s10815-020-01959-4. Epub 2020 Oct 1.
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.
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.
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.
由于夫妻生育年龄推迟到三十多岁和四十多岁，父母年龄导致的生殖能力下降已成为生育的主要障碍。父母年龄较大还与后代神经和心血管疾病发病率增加有关。因此，阐明生殖能力下降的病因具有临床重要性。
在胚胎发育过程中建立了离散卵母细胞库且可能保持休眠数十年的女性中，解读导致生殖能力下降的潜在过程尤其具有挑战性。相反，我们对驱动生殖衰老过程的理解来自对脊椎动物和无脊椎动物等模式生物的研究，这些研究是本文献综述的重点。
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，还有助于识别控制这些变化的主要调节蛋白。在此，我们讨论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。
