Mitochondrial dysfunction in ovarian aging
Shuxin Ma1,2,3,4,5,6, Guangyu Li1,2,3,4,5,6, Yingying Qin2,4,5,6,7,8,9
1Center for Reproductive Medicine, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Abstract:
Mitochondria serve as multifunctional powerhouses within cells, coordinating essential biological activities that are critical for cell viability, including material metabolism, signal transduction, and the maintenance of homeostasis. They support cells in adapting to complex and fluctuating environments. Oocytes, being the largest cells in multicellular organisms, contain a high number of mitochondria with unique structural characteristics. Mitochondria play active roles in the development and maturation of oocytes. A decline in mitochondrial function negatively affects both the quality and quantity of oocytes, thereby contributing to ovarian aging. However, the specific mechanisms through which mitochondrial dysfunction influences the progression of ovarian aging and impacts reproductive longevity remain unclear. Furthermore, medical strategies aimed at rejuvenating mitochondria to restore ovarian reserve and improve female reproductive potential may open new avenues for clinical treatment. In this review, we summarize the current understanding and key evidence regarding the role of mitochondrial dysfunction in ovarian aging and present emerging medical approaches targeting mitochondria to alleviate premature ovarian aging and enhance reproductive performance.
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