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本文引用的文献

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Post-transcriptional and post-translational regulation of Bcl2.Bcl2 的转录后和翻译后调控。
Biochem Soc Trans. 2010 Dec;38(6):1571-5. doi: 10.1042/BST0381571.
2
Ageing and infertility: an overview.衰老与不孕:概述。
Gynecol Endocrinol. 2010 Dec;26(12):855-60. doi: 10.3109/09513590.2010.501889. Epub 2010 Jul 20.
3
mTOR signaling in the control of activation of primordial follicles.mTOR信号通路对原始卵泡激活的调控
Cell Cycle. 2010 May;9(9):1673-4. doi: 10.4161/cc.9.9.11626. Epub 2010 May 25.
4
Gene expression profiles of single human mature oocytes in relation to age.单个人类成熟卵母细胞的基因表达谱与年龄的关系。
Hum Reprod. 2010 Apr;25(4):957-68. doi: 10.1093/humrep/deq014. Epub 2010 Feb 10.
5
Tsc/mTORC1 signaling in oocytes governs the quiescence and activation of primordial follicles.Tsc/mTORC1 信号在卵母细胞中控制原始卵泡的静止和激活。
Hum Mol Genet. 2010 Feb 1;19(3):397-410. doi: 10.1093/hmg/ddp483. Epub 2009 Oct 20.
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Biological versus chronological ovarian age: implications for assisted reproductive technology.生物学年龄与实际年龄:对辅助生殖技术的影响。
Reprod Biol Endocrinol. 2009 Sep 22;7:101. doi: 10.1186/1477-7827-7-101.
7
Genetically modified mouse models for premature ovarian failure (POF).用于卵巢早衰 (POF) 的基因编辑小鼠模型。
Mol Cell Endocrinol. 2010 Feb 5;315(1-2):1-10. doi: 10.1016/j.mce.2009.07.016. Epub 2009 Jul 28.
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Molecular mechanisms underlying the activation of mammalian primordial follicles.哺乳动物原始卵泡激活的分子机制。
Endocr Rev. 2009 Aug;30(5):438-64. doi: 10.1210/er.2008-0048. Epub 2009 Jul 9.
9
Ovarian aging: mechanisms and clinical consequences.卵巢衰老:机制与临床后果
Endocr Rev. 2009 Aug;30(5):465-93. doi: 10.1210/er.2009-0006. Epub 2009 Jul 9.
10
World collaborative report on Assisted Reproductive Technology, 2002.《2002年辅助生殖技术全球协作报告》
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各类卵母细胞老化的细胞与分子机制。

Cellular and molecular mechanisms of various types of oocyte aging.

作者信息

Takahashi Toshifumi, Igarashi Hideki, Amita Mitsuyoshi, Hara Shuichiro, Kurachi Hirohisa

机构信息

Department of Obstetrics and Gynecology Yamagata University Faculty of Medicine 990-9585 Yamagata Japan.

出版信息

Reprod Med Biol. 2011 Jul 2;10(4):239-249. doi: 10.1007/s12522-011-0099-0. eCollection 2011 Dec.

DOI:10.1007/s12522-011-0099-0
PMID:29699098
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5904634/
Abstract

It is well established that age-related decline of a woman's fertility is related to the poor developmental potential of her gametes. The age-associated decline in female fertility is largely attributable to the oocyte aging caused by ovarian aging. Age-associated oocyte aging results in a decrease in oocyte quality. In contrast to ovarian aging, there is a concept of postovulatory oocyte aging. Postovulatory aging of oocytes, not being fertilized for a prolonged time after ovulation, is known to significantly affect the development of oocytes. Both categories of oocyte aging have similar phenotypes of reproductive failure. However, the mechanisms of the decline in oocyte quality are not necessarily equivalent. An age-dependent increase in aneuploidy is a key determinant of oocyte quality. The reduced expression of molecules regulating cell cycle control during meiosis might be involved in the age-dependent increase in aneuploidy. The mechanism of age-associated oocyte aging might be involved in mitochondrial dysfunction, whose etiologies are still unknown. Alternatively, the mechanism of postovulatory oocyte aging might be involved in reactive oxygen species-induced mitochondrial injury pathways followed by abnormal intracellular Ca regulation of the endoplasmic reticulum. We suggest that future research into the mechanism of oocyte aging will be necessary to develop a method to rescue the poor developmental potential of aged oocytes.

摘要

众所周知,女性生育能力随年龄的下降与卵子发育潜力不佳有关。女性生育能力随年龄下降很大程度上归因于卵巢衰老导致的卵母细胞老化。与年龄相关的卵母细胞老化会导致卵母细胞质量下降。与卵巢衰老不同,存在排卵后卵母细胞老化的概念。卵母细胞排卵后老化,即排卵后长时间未受精,已知会显著影响卵母细胞的发育。这两类卵母细胞老化都有类似的生殖失败表型。然而,卵母细胞质量下降的机制不一定相同。非整倍体随年龄增加是卵母细胞质量的关键决定因素。减数分裂过程中调节细胞周期控制的分子表达降低可能与非整倍体随年龄增加有关。与年龄相关的卵母细胞老化机制可能与线粒体功能障碍有关,其病因仍不清楚。或者,排卵后卵母细胞老化机制可能涉及活性氧诱导的线粒体损伤途径,随后是内质网细胞内钙调节异常。我们认为,未来有必要对卵母细胞老化机制进行研究,以开发一种方法来挽救老化卵母细胞不佳的发育潜力。