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31 January 2022 Oocyte mitochondria—key regulators of oocyte function and potential therapeutic targets for improving fertility
Deepak Adhikari, In-won Lee, Wai Shan Yuen, John Carroll
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The development of oocytes and early embryos is dependent on mitochondrial ATP production. This reliance on mitochondrial activity, together with the exclusively maternal inheritance of mitochondria in development, places mitochondria as central regulators of both fertility and transgenerational inheritance mechanisms. Mitochondrial mass and mtDNA content massively increase during oocyte growth. They are highly dynamic organelles and oocyte maturation is accompanied by mitochondrial trafficking around subcellular compartments. Due to their key roles in generation of ATP and reactive oxygen species (ROS), oocyte mitochondrial defects have largely been linked with energy deficiency and oxidative stress. Pharmacological treatments and mitochondrial supplementation have been proposed to improve oocyte quality and fertility by enhancing ATP generation and reducing ROS levels. More recently, the role of mitochondria-derived metabolites in controlling epigenetic modifiers has provided a mechanistic basis for mitochondria–nuclear crosstalk, allowing adaptation of gene expression to specific metabolic states. Here, we discuss the multi-faceted mechanisms by which mitochondrial function influence oocyte quality, as well as longer-term developmental events within and across generations.

Summary Sentence Oocyte mitochondria as potential therapeutic targets.

© The Author(s) 2022. Published by Oxford University Press on behalf of Society for the Study of Reproduction. All rights reserved. For permissions, please e-mail:
Deepak Adhikari, In-won Lee, Wai Shan Yuen, and John Carroll "Oocyte mitochondria—key regulators of oocyte function and potential therapeutic targets for improving fertility," Biology of Reproduction 106(2), 366-377, (31 January 2022).
Received: 12 January 2022; Accepted: 4 February 2021; Published: 31 January 2022
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