Mitochondria in Ovarian Aging and Reproductive Longevity

Ageing Res Rev. 2020 Nov:63:101168. doi: 10.1016/j.arr.2020.101168. Epub 2020 Sep 4.

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.

Keywords: Infertility; Mitochondrial DNA; Mitochondrial dysfunction; Mitochondrial therapies; Ovarian aging; Reproductive longevity.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aging / genetics
  • DNA, Mitochondrial / genetics
  • DNA, Mitochondrial / metabolism
  • Humans
  • Longevity*
  • Mitochondria* / genetics
  • Oocytes / metabolism

Substances

  • DNA, Mitochondrial