Dysregulation of CREB5 Impairs Decidualization and Maternal-Fetal Interactions by Inhibiting Autophagy in Recurrent Spontaneous Abortion.

Zhidian LiFangfang DaiRonghui ZhuYuwei ZhangJing ChenLiping ChenHua LiuYan-Xiang Cheng

Published in: Reproductive sciences (Thousand Oaks, Calif.) (2024)

Our data support the supposition that CREB5 disturbs the decidualization of endometrial stromal cells and interactions at the maternal-fetal interface by inhibiting autophagy and that its abnormal upregulation and dysfunction may lead to RSA. It may function as a diagnostic and therapeutic target for RSA. Similarly, we found that in the spontaneous abortion mouse model, the expression of CREB5 in the decidual tissue of the abortion group was significantly increased, and autophagy was decreased.

Keyphrases

signaling pathway
cell death
endoplasmic reticulum stress
oxidative stress
poor prognosis
mouse model
birth weight
pregnancy outcomes
cell proliferation
pregnant women
machine learning
long non coding rna
endometrial cancer
binding protein
physical activity
preterm birth
data analysis