长寿
线粒体DNA
线粒体
生物
不育
卵母细胞
生育率
生物信息学
生理学
男科
遗传学
医学
胚胎
怀孕
人口
基因
环境卫生
作者
Jasmine L. Chiang,Pallavi Shukla,Kelly Pagidas,Noha S. Ahmed,Srinivasu Karri,Deidre Gunn,William W. Hurd,Keshav K. Singh
标识
DOI:10.1016/j.arr.2020.101168
摘要
Mitochondrial dysfunction is one of the hallmarks of aging. Consistently mitochondrial DNA (mtDNA) copy number and function decline with age in various tissues. There is increasing evidence to support that mitochondrial dysfunction drives ovarian aging. A decreased mtDNA copy number is also reported during ovarian aging. However, the mitochondrial mechanisms contributing to ovarian aging and infertility are not fully understood. Additionally, investigations into mitochondrial therapies to rejuvenate oocyte quality, select viable embryos and improve mitochondrial function may help enhance fertility or extend reproductive longevity in the future. These therapies include the use of mitochondrial replacement techniques, quantification of mtDNA copy number, and various pharmacologic and lifestyle measures. This review aims to describe the key evidence and current knowledge of the role of mitochondria in ovarian aging and identify the emerging potential options for therapy to extend reproductive longevity and improve fertility.
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