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卵巢卵泡衰老的细胞和分子层面

Cellular and molecular aspects of ovarian follicle ageing.

作者信息

Tatone Carla, Amicarelli Fernanda, Carbone Maria Cristina, Monteleone Patrizia, Caserta Donatella, Marci Roberto, Artini Paolo Giovanni, Piomboni Paola, Focarelli Riccardo

机构信息

Department of Biomedical Sciences and Technologies, University of L'Aquila, L'Aquila, Via Vetoio 67100, Italy.

出版信息

Hum Reprod Update. 2008 Mar-Apr;14(2):131-42. doi: 10.1093/humupd/dmm048. Epub 2008 Jan 31.

DOI:10.1093/humupd/dmm048
PMID:18239135
Abstract

It is well established that age-related decline of the biological capacity of a woman to reproduce is primarily related to the poor developmental potential of her gametes. This renders female ageing the most significant determinant of success in IVF. Starting with a reference picture of the main molecular and cellular failures of aged oocytes, granulosa cells and follicular microenvironment, this review focuses on age-related biochemical mechanisms underlying these changes. According to the most relevant concept of ageing, age-associated malfuction results from physiological accumulation of irreparable damage to biomolecules as an unavoidable side effect of normal metabolism. More than a decade after the free radical theory of ovarian ageing, biological and clinical research supporting the involvement of oxidative injuries in follicle ageing is discussed. Looking for the aetiology of oxidative stress, we consider the effect of ageing on ovarian and follicular vascularization. Then, we propose a potential role of advanced glycation end-products known to be involved in the physiological ageing of most tissues and organs. We conclude that future investigation of age-related molecular damage in the different ovarian components will be imperative in order to evaluate the possibility to save or rescue the developmental potential of aged oocytes.

摘要

众所周知,女性生殖生物能力随年龄增长而下降,这主要与卵子发育潜力差有关。这使得女性年龄成为体外受精成功的最重要决定因素。本文从老年卵母细胞、颗粒细胞和卵泡微环境的主要分子和细胞缺陷的参考图开始,重点关注这些变化背后与年龄相关的生化机制。根据最相关的衰老概念,与年龄相关的功能障碍是正常代谢不可避免的副作用,即生物分子受到不可修复损伤的生理积累所致。在卵巢衰老的自由基理论提出十多年后,本文讨论了支持氧化损伤参与卵泡衰老的生物学和临床研究。在寻找氧化应激的病因时,我们考虑了衰老对卵巢和卵泡血管生成的影响。然后,我们提出了晚期糖基化终产物的潜在作用,已知其参与大多数组织和器官的生理性衰老。我们得出结论,为了评估拯救或挽救老年卵母细胞发育潜力的可能性,未来对卵巢不同成分中与年龄相关的分子损伤进行研究将势在必行。

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