National Institutes of Health, NICHD, and Washington Hospital Center, Washington, DC, USA.
Semin Reprod Med. 2011 Jul;29(4):283-98. doi: 10.1055/s-0031-1280914. Epub 2011 Oct 4.
Primary ovarian insufficiency (POI), also known as premature ovarian failure, is a form of hypergonadotropic hypogonadism that causes infertility in ~1% of women <40 years of age. POI has important health consequences for affected patients; however, the mechanisms that cause ovarian dysfunction are poorly understood. Elucidating these mechanisms is paramount to developing better testing and treatment strategies for affected girls and women. For obvious reasons, studies looking directly at the human ovary are extremely limited. Recently, numerous genetically engineered mouse models have been developed to investigate the molecular mechanisms that may be involved in the pathogenesis of POI. Two potential mechanisms may be involved in the development of POI: (1) abnormalities in primordial follicle activation and (2) increased rates of apoptosis of oocytes. Each of these mechanisms may lead to early depletion of ovarian follicular reserve, and thus be a contributing factor in POI. This review addresses current knowledge of molecular mechanisms controlling primordial follicle activation and oocyte apoptosis, as evidenced from various genetic mouse models. Translation of these data into clinically effective treatments or even prevention strategies may improve fertility and quality of life for women with this form of reproductive dysfunction.
原发性卵巢功能不全（POI），也称为卵巢早衰，是一种高促性腺激素性性腺功能减退症，导致约 1%的<40 岁女性不孕。POI 对受影响的患者有重要的健康后果；然而，导致卵巢功能障碍的机制尚不清楚。阐明这些机制对于开发针对受影响女孩和妇女的更好的检测和治疗策略至关重要。由于显而易见的原因，直接研究人类卵巢的研究极为有限。最近，已经开发出许多基因工程小鼠模型来研究可能参与 POI 发病机制的分子机制。两种潜在的机制可能参与 POI 的发展：（1）原始卵泡激活异常和（2）卵母细胞凋亡率增加。这些机制中的每一种都可能导致卵巢卵泡储备的早期耗尽，因此是 POI 的一个促成因素。这篇综述讨论了从各种遗传小鼠模型中得出的控制原始卵泡激活和卵母细胞凋亡的分子机制的最新知识。将这些数据转化为临床有效的治疗方法，甚至预防策略，可能会提高患有这种生殖功能障碍的女性的生育能力和生活质量。
