Molecular Neurobiology Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Department of Human Physiology and Pathophysiology, Collegium Medicum, University of Warmia and Mazury, 10-719 Olsztyn, Poland.
Cells. 2022 Aug 22;11(16):2612. doi: 10.3390/cells11162612.
While at the organismal level, biological aging can be estimated by telomere length and DNA methylation signatures, reliable biomarkers that can predict reproductive age are much needed to gauge the quality of an oocyte. Reproductive medicine and fertility centers often merely quantitate the ovarian reserve to predict the likelihood of fertilization and pregnancy in women of advanced reproductive age. It is highly important to address the level of age-related decline in oocyte quality since it leads to an increased risk of miscarriages and aneuploidy. Conversely, the pathways behind oocyte aging remain, in large part, elusive. Telomere shortening upon chronic stress exposure regulates mitochondria function and biogenesis by various pathways; therefore, establishing a link between these two important players and extrapolating them for the aging of oocytes will be the purpose of our commentary.
虽然在机体水平上，可以通过端粒长度和 DNA 甲基化特征来估计生物衰老，但仍需要可靠的生物标志物来预测生殖年龄，以评估卵子的质量。生殖医学和生育中心通常只是定量卵巢储备，以预测高龄妇女受精和怀孕的可能性。重要的是要解决卵母细胞质量随年龄下降的问题，因为这会增加流产和非整倍体的风险。相反，卵母细胞衰老的途径在很大程度上仍然难以捉摸。慢性应激暴露导致端粒缩短，通过多种途径调节线粒体功能和生物发生；因此，建立这两个重要因素之间的联系，并将其推断为卵母细胞的衰老，将是我们评论的目的。
