PDF(Pubmed)
Abstract：
Endometrial receptivity is a state of the endometrium defined by its readiness for embryo implantation. When the receptivity of the endometrium is impaired due to hyperandrogenism or androgen excess, this condition can lead to pregnancy loss or infertility. Hyperandrogenism encompasses a wide range of clinical manifestations, including polycystic ovary syndrome (PCOS), idiopathic hirsutism, hirsutism and hyperandrogaenemia, non-classical congenital adrenal hyperplasia, hyperandrogenism, insulin resistance, acanthosis nigricans (HAIR-AN), ovarian or adrenal androgen-secreting neoplasms, Cushing\'s syndrome, and hyperprolactinaemia. Recurrent miscarriages have been shown to be closely related to elevated testosterone levels, which alter the endometrial milieu so that it is less favourable for embryo implantation. There are mechanisms for endometrial receptivity that are affected by excess androgen. The HOXA gene, aVβ3 integrin, CDK signalling pathway, MECA-79, and MAGEA-11 were the genes and proteins affect endometrial receptivity in the presence of a hyperandrogenic state. In this review, we would like to explore the other manifestations of androgen excess focusing on causes other than PCOS and learn possible mechanisms of endometrial receptivity behind androgen excess leading to pregnancy loss or infertility.
摘要：
子宫内膜容受性是子宫内膜的一种状态，由其准备胚胎植入来定义。当子宫内膜的容受性由于高雄激素血症或雄激素过量而受损时，这种情况会导致怀孕失败或不孕。雄激素过多症包括广泛的临床表现，包括多囊卵巢综合征（PCOS），特发性多毛症,多毛症和高雄激素症，非经典先天性肾上腺增生，雄激素过多症,胰岛素抵抗，黑棘皮病（Hair-AN），卵巢或肾上腺分泌雄激素的肿瘤，库欣综合征,和高催乳素血症.复发性流产已被证明与睾丸激素水平升高密切相关，这改变了子宫内膜环境，因此对胚胎植入不利。存在受过量雄激素影响的子宫内膜容受性的机制。HOXA基因,αVβ3整合素，CDK信号通路，MECA-79和MAGEA-11是在高雄激素状态下影响子宫内膜容受性的基因和蛋白质。在这次审查中,我们想探讨雄激素过剩的其他表现,重点关注PCOS以外的原因,并了解雄激素过剩导致妊娠流产或不孕背后的子宫内膜容受性的可能机制.
