【摘要】 原始卵泡激活是女性生殖的关键步骤，但原始卵泡被过度激活会引发原始卵泡库过早耗竭而导致早发性卵巢功能不全。原始卵泡受到过度抑制时维持在休眠状态，无法正常地发育成熟而导致女性无法自然排卵，临床上表现为原发性不孕。因此，探索原始卵泡在静止期被激活的分子机制，调节其过度激活或过度抑制的状态，对于维护女性生育能力具有至关重要的意义。细胞生长受到细胞周期蛋白(cyclin, CCN)和细胞周期蛋白依赖激酶(cyclin-dependent kinase, CDK)家族的调控。越来越多的研究表明CCN和CDK通过PI3K/AKT等信号通路参与原始卵泡激活。CCN和CDK是卵泡发育过程中卵巢颗粒细胞增殖所必需的调控因子。本文就原始卵泡激活相关CCN和CDK的研究进展进行综述，为揭示原始卵泡激活分子机制及临床助孕提供理论依据。更多还原

【Abstract】 Primordial follicle activation is a critical step in female reproduction, and overactivation of primordial follicles triggers premature depletion of the primordial follicle bank, resulting in premature ovarian insufficient. When primitive follicles are excessively inhibited, they remain in a dormant state, unable to grow and mature normally, ultimately leading to atresia and female infertility characterized by primary infertility. Therefore, exploring the molecular mechanisms that activate follicles during quiescence and regulating their states of excessive activation or inhibition are of utmost importance for maintaining female fertility. Cell growth is dependent on the regulation of cyclin(CCN) and cyclin-dependent kinase(CDK). More and more studies have shown that CCN and CDK participate in primordial follicle activation via signaling pathways such as PI3K/AKT. And CCN and CDK are essential regulators of granulosa cells proliferation during follicle development. We reviewed the research progress of CCN and CDK related to primitive follicle activation, so as to provide a theoretical basis for revealing the molecular mechanism of primitive follicle activation and clinical fertility.更多还原