线粒体
衰老
卵母细胞
线粒体DNA
生物
细胞生物学
生物信息学
DNA损伤
医学
遗传学
胚胎
基因
DNA
作者
Wenhan Ju,Yuewen Zhao,Yi Yu,Shuai Zhao,Shan Xiang,Fang Lian
标识
DOI:10.3389/fendo.2024.1361289
摘要
Mitochondria plays an essential role in regulating cellular metabolic homeostasis, proliferation/differentiation, and cell death. Mitochondrial dysfunction is implicated in many age-related pathologies. Evidence supports that the dysfunction of mitochondria and the decline of mitochondrial DNA copy number negatively affect ovarian aging. However, the mechanism of ovarian aging is still unclear. Treatment methods, including antioxidant applications, mitochondrial transplantation, emerging biomaterials, and advanced technologies, are being used to improve mitochondrial function and restore oocyte quality. This article reviews key evidence and research updates on mitochondrial damage in the pathogenesis of ovarian aging, emphasizing that mitochondrial damage may accelerate and lead to cellular senescence and ovarian aging, as well as exploring potential methods for using mitochondrial mechanisms to slow down aging and improve oocyte quality.
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