自噬反应在慢性子宫内膜炎发病中的潜在作用

慢性子宫内膜炎（chronic endometritis,CE）可引起不孕症、复发性流产和反复植入失败等不良生殖预后,其发病机制尚未阐明。CE患者的子宫内膜组织中存在异常的自噬反应,提示自噬在CE发病中发挥重要作用。研究发现,CE的发生与巨噬细胞分布、极化异常以及NOD样受体蛋白3（NOD-like receptor protein 3,NLRP3）炎症小体的异常激活密切相关。而且,巨噬细胞极化以及NLRP3炎症小体的组装和激活均受自噬反应调控。因此,自噬反应可能通过调节巨噬细胞极化影响NLRP3炎症小体激活,从而参与CE的发生。上述观点为CE发病机制提供了新的认识,也为其治疗提供了潜在的新靶点。

Potential Role of Autophagy in the Pathogenesis of Chronic Endometritis

Chronic endometritis (CE) can lead to infertility, recurrent pregnancy loss and recurrent implantation failure. The specific pathogenesis mechanism of CE remains unknown. Abnormal autophagy was proved in the endometrium of patients with CE, indicating that autophagy plays an important role in the development of CE. Researches have confirmed that the development of CE is related with abnormal distribution and polarization of macrophages, as well as abnormal activation of NOD-like receptor protein 3 (NLRP3) inflammasome, both of which are modulated by autophagy. Thus, we propose that autophagy may activate NLRP3 inflammasome by regulating macrophage polarization, thereby leading to the occurrence of CE. This review illustrates a new insight for the pathogenesis of CE and provides new potential targets for the treatment of CE.