| Literature DB >> 32896666 |
Jasmine L Chiang1, Pallavi Shukla2, Kelly Pagidas3, Noha S Ahmed4, Srinivasu Karri5, Deidre D Gunn1, William W Hurd1, Keshav K Singh6.
Abstract
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.Entities:
Keywords: Infertility; Mitochondrial DNA; Mitochondrial dysfunction; Mitochondrial therapies; Ovarian aging; Reproductive longevity
Mesh：
Substances：
Year: 2020 PMID： 32896666 PMCID： PMC9375691 DOI： 10.1016/j.arr.2020.101168
Source DB: PubMed Journal: Ageing Res Rev ISSN： 1568-1637 Impact factor: 11.788