Department of Medical Biochemistry and Biophysics, Umeå University, SE-901 87 Umeå, Sweden.
Mol Cell Endocrinol. 2010 Feb 5;315(1-2):1-10. doi: 10.1016/j.mce.2009.07.016. Epub 2009 Jul 28.
Premature ovarian failure (POF) is a complex disorder that affects approximately 1% of women. POF is characterized by the depletion of functional ovarian follicles before the age of 40 years, and clinically, patients may present with primary amenorrhea or secondary amenorrhea. Although some genes have been hypothesized to be candidates responsible for POF, the etiology of most of the cases is idiopathic, with the underlying causes still unidentified because of the heterogeneity of the disease. In this review, we consider some mutant mouse models that exhibit phenotypes which are comparable to human POF, and we suggest that the use of these mouse models may help us to gain a better understanding of the molecular mechanisms underlying POF in humans.
卵巢早衰（POF）是一种复杂的疾病，影响约 1%的女性。POF 的特征是在 40 岁之前功能性卵泡耗竭，临床上患者可能表现为原发性闭经或继发性闭经。虽然一些基因被假设为导致 POF 的候选基因，但大多数病例的病因是特发性的，由于疾病的异质性，其潜在原因仍未确定。在这篇综述中，我们考虑了一些表现出与人类 POF 相当的表型的突变小鼠模型，并认为这些小鼠模型的使用可能有助于我们更好地理解人类 POF 的分子机制。
