Mitochondria: the epigenetic regulators of ovarian aging and longevity.
Abstract
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-KG. 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.
The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.
Research summary
The paper addresses the role of mitochondria and epigenetic regulation in ovarian aging, which is directly related to the biological mechanisms of aging and longevity. It discusses potential strategies to enhance mitochondrial function to preserve ovarian health, indicating a focus on addressing root causes of aging rather than merely treating symptoms. However, while the findings are solid and contribute to the understanding of ovarian aging, they do not present groundbreaking insights that would significantly advance the field of longevity research, hence the moderate impact score.
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