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Mitochondria in Ovarian Aging and Reproductive Longevity. | LitMetric

Mitochondria in Ovarian Aging and Reproductive Longevity.

Ageing Res Rev

Department of Genetics, University of Alabama at Birmingham, Kaul Genetics Building Room 630, 720 20(th)Street South, Birmingham, AL, 35294, United States; UAB Department of Genetics, Center for Women's Reproductive Health, Kaul Genetics Building University of Alabama at Birmingham, Room 620, 720 20(th)Street South, Birmingham, AL, 35294, United States. Electronic address:

Published: November 2020

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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9375691PMC
http://dx.doi.org/10.1016/j.arr.2020.101168DOI Listing

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