自噬在排卵障碍性不孕症中的作用

排卵障碍性不孕症是临床中常见的不孕症类型，是由于患者存在内分泌紊乱、染色体和基因异常、药物损伤和卵巢病变等因素导致无排卵或稀发排卵，影响精子与卵子的结合，最终导致不孕。自噬是细胞内组分降解与再利用的重要方式，存在于多种生理和病理过程中，包括卵巢储备、卵泡发育和闭锁等。研究表明，引起排卵障碍的多种疾病中存在卵巢内自噬异常：多囊卵巢综合征中自噬活性升高，早发性卵巢功能不全和卵巢早衰中自噬水平异常增加或减少，卵巢子宫内膜异位囊肿中自噬处于抑制状态。包括哺乳动物雷帕霉素靶蛋白在内的多种信号通路参与调控卵泡颗粒细胞和卵母细胞中的自噬。自噬关键因子的缺失和突变，以及过度激活均会影响颗粒细胞的增殖、凋亡和分泌功能，从而阻碍卵泡正常发育和排卵。二甲双胍和一些激素类药物能够参与自噬过程的调节。总之，自噬在排卵障碍性不孕症的发生过程中起重要的调控作用。

Autophagy in Mechanism of Ovulatory Dysfunction Infertility

Ovulatory dysfunction infertility, a common type of infertility, is due to the anovulation or oligo-ovulation because of endocrine disorders, chromosomal and genetic abnormalities, drug toxicity, ovarian lesions and other factors, which affect the combination of sperm and oocytes. Autophagy is an important way for the degradation and reuse of cell components. It occurs in a variety of physiological and pathological processes, including ovarian reserve, follicular development and atresia. Studies have shown that the abnormal autophagy in the ovary results in a variety of diseases causing ovulation disorders. For example, the autophagy activity is increased in polycystic ovary syndrome, abnormally increased or decreased in premature ovarian insufficiency and premature ovarian failure, and suppressed in ovarian endometriosis cysts. Multiple signaling pathways including mTOR are involved in the regulation of autophagy in follicular granulosa cells and oocytes. Deletion and mutation of key autophagy factors, as well as over activation, affect the proliferation, apoptosis and secretion of follicular cells, thus hindering the normal development and ovulation of follicles. Metformin and some hormone drugs can participate in the regulation of autophagy. In conclusion, autophagy may play a role in the development of ovulatory dysfunction infertility.