The ovaries exhibit significant age-related loss of function somewhat ahead of the rest of the body. Why is this the case? There is no good answer at present as to why the underlying mechanisms of aging produce a faster decline in the ovaries. The ability to compare the biochemistry of aging in the ovaries with the biochemistry of aging in the rest of the body may be an opportunity to learn something about aging more generally, however. So one sees papers such as this one, in which researchers review what is known of the mitochondrial dysfunction associated with aging specifically in the ovaries versus its role in aging elsewhere in the body.
Ovarian aging is a major health concern for women. Ovarian aging is associated with reduced health span and longevity. Mitochondrial dysfunction is one of the hallmarks of ovarian aging. In addition to providing oocytes with optimal energy, the mitochondria provide a co-substrate that drives epigenetic processes. Studies show epigenetic alterations, both nuclear and mitochondrial contribute to ovarian aging. Both, nuclear and mitochondrial genomes cross-talk with each other, resulting in two ways orchestrated anterograde and retrograde response that involves epigenetic changes in nuclear and mitochondrial compartments.
Epigenetic alterations causing changes in metabolism impact ovarian function. Key mitochondrial co-substrate includes acetyl CoA, NAD+, ATP, and α-ketoglutarate. Thus, enhancing mitochondrial function in aging ovaries may preserve ovarian function and can lead to ovarian longevity and reproductive and better health outcomes in women. This article describes the role of mitochondria-led epigenetics involved in ovarian aging and discusses strategies to restore epigenetic reprogramming in oocytes by preserving, protecting, or promoting mitochondrial function.
Link: https://doi.org/10.3389/fendo.2024.1424826
View the full article at FightAging
