The role of mitophagy during oocyte aging in human, mouse, and Drosophila: implications for oocyte quality and mitochondrial disease
There is a worldwide trend for women to have their first pregnancy later in life. However, as oocyte quality declines with maternal aging, this trend leads to an increase in subfertility. The cellular mechanisms underlying this decline in oocyte competence are poorly understood. Oocyte mitochondria...
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Bioscientifica
2021
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oai:doaj.org-article:d5f1cc22b08d443fb09b17924209ee022021-11-10T08:39:11ZThe role of mitophagy during oocyte aging in human, mouse, and Drosophila: implications for oocyte quality and mitochondrial diseasehttps://doi.org/10.1530/RAF-21-00602633-8386https://doaj.org/article/d5f1cc22b08d443fb09b17924209ee022021-11-01T00:00:00Zhttps://raf.bioscientifica.com/view/journals/raf/2/4/RAF-21-0060.xmlhttps://doaj.org/toc/2633-8386There is a worldwide trend for women to have their first pregnancy later in life. However, as oocyte quality declines with maternal aging, this trend leads to an increase in subfertility. The cellular mechanisms underlying this decline in oocyte competence are poorly understood. Oocyte mitochondria are the subcellular organelles that supply the energy that drives early embryogenesis, and thus their quality is critical for successful conception. Mitochondria contain their own DNA (mtDNA) and mutations in mtDNA cause mitochondrial diseases with severe symptoms, such as neurodegeneration and heart disease. Since mitochondrial function declines in tissues as humans age accompanied by an accumulation of mtDNA mutations, mtDNA is implicated as a cause of declining oocyte quality in older mothers. While this mutation load could be caused by declining accuracy of the mitochondrial replisome, age-related decline in mitochondrial quality control likely contributes, however knowledge is lacking. Mitophagy, a cellular process which specifically targets and recycles damaged mitochondria may be involved, but studies are scarce. And although assisted reproductive technologies can help older mothers, how these techniques affect the mechanisms that regulate mitochondrial and oocyte quality have not been studied. With the long-term goal of understanding the molecular mechanisms that control mitochondrial quality in the oocyte, model systems including Drosophila and mouse as well as human oocytes have been used. In this review, we explore the contribution of mitophagy to oocyte quality and the need for further systematic investigation in oocytes during maternal aging using different systems.Rachel T CoxJoanna PoultonSuzannah A WilliamsBioscientificaarticlemitophagymitochondriaovaryoocytedrosophilamousehumanmtdnaartsReproductionQH471-489Gynecology and obstetricsRG1-991ENReproduction and Fertility, Vol 2, Iss 4, Pp R113-R129 (2021) |
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mitophagy mitochondria ovary oocyte drosophila mouse human mtdna arts Reproduction QH471-489 Gynecology and obstetrics RG1-991 |
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mitophagy mitochondria ovary oocyte drosophila mouse human mtdna arts Reproduction QH471-489 Gynecology and obstetrics RG1-991 Rachel T Cox Joanna Poulton Suzannah A Williams The role of mitophagy during oocyte aging in human, mouse, and Drosophila: implications for oocyte quality and mitochondrial disease |
description |
There is a worldwide trend for women to have their first pregnancy later in life. However, as oocyte quality declines with maternal aging, this trend leads to an increase in subfertility. The cellular mechanisms underlying this decline in oocyte competence are poorly understood. Oocyte mitochondria are the subcellular organelles that supply the energy that drives early embryogenesis, and thus their quality is critical for successful conception. Mitochondria contain their own DNA (mtDNA) and mutations in mtDNA cause mitochondrial diseases with severe symptoms, such as neurodegeneration and heart disease. Since mitochondrial function declines in tissues as humans age accompanied by an accumulation of mtDNA mutations, mtDNA is implicated as a cause of declining oocyte quality in older mothers. While this mutation load could be caused by declining accuracy of the mitochondrial replisome, age-related decline in mitochondrial quality control likely contributes, however knowledge is lacking. Mitophagy, a cellular process which specifically targets and recycles damaged mitochondria may be involved, but studies are scarce. And although assisted reproductive technologies can help older mothers, how these techniques affect the mechanisms that regulate mitochondrial and oocyte quality have not been studied. With the long-term goal of understanding the molecular mechanisms that control mitochondrial quality in the oocyte, model systems including Drosophila and mouse as well as human oocytes have been used. In this review, we explore the contribution of mitophagy to oocyte quality and the need for further systematic investigation in oocytes during maternal aging using different systems. |
format |
article |
author |
Rachel T Cox Joanna Poulton Suzannah A Williams |
author_facet |
Rachel T Cox Joanna Poulton Suzannah A Williams |
author_sort |
Rachel T Cox |
title |
The role of mitophagy during oocyte aging in human, mouse, and Drosophila: implications for oocyte quality and mitochondrial disease |
title_short |
The role of mitophagy during oocyte aging in human, mouse, and Drosophila: implications for oocyte quality and mitochondrial disease |
title_full |
The role of mitophagy during oocyte aging in human, mouse, and Drosophila: implications for oocyte quality and mitochondrial disease |
title_fullStr |
The role of mitophagy during oocyte aging in human, mouse, and Drosophila: implications for oocyte quality and mitochondrial disease |
title_full_unstemmed |
The role of mitophagy during oocyte aging in human, mouse, and Drosophila: implications for oocyte quality and mitochondrial disease |
title_sort |
role of mitophagy during oocyte aging in human, mouse, and drosophila: implications for oocyte quality and mitochondrial disease |
publisher |
Bioscientifica |
publishDate |
2021 |
url |
https://doi.org/10.1530/RAF-21-0060 https://doaj.org/article/d5f1cc22b08d443fb09b17924209ee02 |
work_keys_str_mv |
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