Abstract：
Mitochondrial quality control plays a critical role in cytogenetic development by regulating various cell-death pathways and modulating the release of reactive oxygen species (ROS). Dysregulated mitochondrial quality control can lead to a broad spectrum of diseases, including reproductive disorders, particularly female infertility. Ovarian insufficiency is a significant contributor to female infertility, given its high prevalence, complex pathogenesis, and profound impact on women\'s health. Understanding the pathogenesis of ovarian insufficiency and devising treatment strategies based on this understanding are crucial. Oocytes and granulosa cells (GCs) are the primary ovarian cell types, with GCs regulated by oocytes, fulfilling their specific energy requirements prior to ovulation. Dysregulation of mitochondrial quality control through gene knockout or external stimuli can precipitate apoptosis, inflammatory responses, or ferroptosis in both oocytes and GCs, exacerbating ovarian insufficiency. This review aimed to delineate the regulatory mechanisms of mitochondrial quality control in GCs and oocytes during ovarian development. This study highlights the adverse consequences of dysregulated mitochondrial quality control on GCs and oocyte development and proposes therapeutic interventions for ovarian insufficiency based on mitochondrial quality control. These insights provide a foundation for future clinical approaches for treating ovarian insufficiency.
摘要：
线粒体质量控制通过调节各种细胞死亡途径和调节活性氧（ROS）的释放在细胞遗传学发育中起关键作用。线粒体质量控制失调会导致广泛的疾病，包括生殖障碍，尤其是女性不孕症。卵巢功能不全是女性不孕症的重要原因，鉴于其患病率高，复杂的发病机制，并对妇女的健康产生深远的影响。了解卵巢功能不全的发病机制并在此基础上制定治疗策略至关重要。卵母细胞和颗粒细胞（GC）是主要的卵巢细胞类型，由卵母细胞调节的GCs，在排卵前满足他们的特定能量需求。通过基因敲除或外界刺激引起的线粒体质量控制失调可导致细胞凋亡,炎症反应，或在卵母细胞和GC中的铁细胞凋亡，加重卵巢功能不全。本文旨在探讨卵巢发育过程中GCs和卵母细胞线粒体质量控制的调控机制。这项研究强调了线粒体质量控制失调对GC和卵母细胞发育的不利影响，并提出了基于线粒体质量控制的卵巢功能不全的治疗干预措施。这些见解为未来治疗卵巢功能不全的临床方法提供了基础。
