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p53 介导蜕膜化受损致复发性流产的研究进展. (Chinese)
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- Author(s): 王炜; 赵小萱; 古玥儒; 常卓; 冯晓玲
- Source:
Journal of International Reproductive Health/Family Planning; sep2018, Vol. 37 Issue 5, p430-434, 5p
- Additional Information
- Alternate Title:
Recurrent Spontaneous Abortion due to the Damaged Decidualization by p53. (English)
- 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. [ABSTRACT FROM AUTHOR]
- Abstract:
复发性流产(RSA)病因复杂,约50%的RSA患者病因不明,其中由于蜕膜化受损所致的胚胎 反复丢失成为学者关注的焦点。p53通过参与多种信号通路介导蜕膜化受损从而引发RSA。其中p53/p21信号 通路过度激活可干扰细胞周期调控因子的表达,使细胞周期进入停滞状态,蜕膜多倍体化障碍,转而促进细 胞凋亡,影响胚胎着床。而在雌二醇(E2)/p53-白血病抑制因子(LIF)-信号转导和转录激活因子3(STAT3)信 号通路中,p53在雌激素的协同作用下促进植入期子宫内膜腺体分泌LIF,并激活JAK/STAT信号通路,为胚胎 着床创造有利条件。研究表明,参与调控p53信号通路的长链非编码RNA(lncRNA)功能异常及p53通路基因多 态性均可影响p53的活性,从而影响蜕膜化及妊娠结局。现就近年来国内外p53蛋白家族及其通路参与蜕膜化 的相关研究进行综述。 [ABSTRACT FROM AUTHOR]
- Abstract:
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