关键词: 流产, 习惯性, 蜕膜, 基因, p53, 肿瘤抑制蛋白质p53, 胚胎植入

Abstract: The etiology of recurrent spontaneous abortion (RSA) is very complex, and about 50% of cases are undefined. The repeated loss of the embryo caused by the damaged decidualization is a research hotspot. p53 mediates the deterioration of decidualization by participating in multiple signaling pathways, leading to recurrent abortion. The excessive activation of p53/p21 signaling pathway can interfere the expressions of those regulatory factors related to cell cycle which make the blockage of cell cycle, induce the decidualization, promote the apoptosis, and affect the embryonic implantation. In the E2/p53-leukemia inhibitory factor (LIF)-signal transduction and transcriptional activator factor 3 (STAT3) signaling pathway, p53 promotes the secretion of LIF by the endometrial gland during the implantation period under the synergistic effect of estrogen, and activates JAK/STAT signaling pathway, creating favorable conditions for embryonic implantation. Moreover, studies have shown that the functional abnormality of lncRNA involved in regulating p53 signaling pathway and the polymorphism of p53 pathway genes could affect the activity of p53, and decidualization and pregnancy outcome. The recent studies on p53 protein family and its pathways involved in decidualization were reviewed.

Key words: Abortion, habitual, Decidua, Genes, p53, Tumor suppressor protein p53, Embryo implantation