Mitochondria are the power plants of the cell, their production of the chemical energy store molecule adenosine triphosphate (ATP) essential to cell function. With advancing age mitochondria become dysfunctional for reasons that in part involve damage to mitochondrial DNA and in part involve changes in gene expression that harm mitochondrial structure and the quality control processes of mitophagy. Mitochondrial dysfunction places stress on cells in a number of ways, from loss of ATP production to increased generation of oxidative molecules. What might be fixed if mitochondria could be restored to a more youthful state of function, and how might that goal be achieved? Researchers here look at these questions in the context of the aging of the ovaries.
Ovarian aging is a complex process characterized by a gradual decline in both the quantity and quality of oocytes. This age-related decline in ovarian function not only results in reduced fertility and an increased risk of pregnancy complications but also significantly impacts critical elements like hormonal balance, bone health, cardiovascular well-being, and cognitive function.
Mitochondria assume a fundamental role in energy generation through oxidative phosphorylation. Considering that the oocyte is the body's most mitochondria-rich cell, these organelles bear significant responsibility in fostering its development, promoting follicular growth, and orchestrating hormone regulation - all crucial factors in ensuring successful reproduction. While several other factors, such as vascular network defects, hormonal dysregulation, genetic and epigenetic alterations, and environmental and lifestyle influences, have been identified as contributing to the aging of the ovary, mitochondrial dysfunction appears to be a more central and significant driver of this process. Moreover, preserving mitochondrial function not only holds promise for enhancing reproductive outcomes but also for delaying aging in women. Exploring therapeutic strategies targeted at maintaining mitochondrial health could offer significant opportunities for addressing age-related fertility decline and promoting reproductive and overall well-being in women.
In this review, we focus on the intricate interplay between mitochondrial function and ovarian aging, and the mechanisms through which mitochondrial health affects oocyte and ovarian follicle quality, and how it contributes to age-related fertility decline. Furthermore, we explore potential therapeutic strategies aimed at preserving mitochondrial function to enhance reproductive outcomes for women as they age.
Link: https://doi.org/10.3...do.2024.1417007
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