The purpose of this study is to explore the role and mechanism in endometrial receptivity and RIF
In vitro fertilization-embryo transfer (IVF-ET) is a commonly used and has enhanced the possibilities for treatmenting infertility successfully. However, the repeated implantation failure (RIF) is a key problem affecting further improvement of clinical pregnancy rates. The etiology of RIF is complex and highly heterogeneous, including immunology, thrombophilias, endometrial receptivity, microbiome, anatomical abnormalities, male factors, and embryo aneuploidy. Among them, abnormal endometrial receptivity is one of the key factors leading to RIF, and about two-thirds of implant failures are caused by decreased endometrial receptivity . In addition to the cyclical changes in endometrium morphology, increasing evidence indicated that there exists a very complex network for regulation of endometrial receptivity and implantation, including gene expression, protein modification, and miRNAs regulation. However, it still remains unclear about the regulatory mechanism for endometrial receptivity. The cell fate decisions underlying this important biological process are made at the level of single cells. Despite the apparent synchrony in cellular systems, single cell analysis results show that even the same cell line or tissue, can present different genomes, transcriptomes, and epigenomes during cell division and differentiation. Recent technological advances have enabled the gene-expression profiles of individual cells to be measured by single-cell RNA sequencing (scRNA-seq), providing a new opportunity to define the cell types and molecular pathways that are involved in tissue homeostasis and disease with high precision . We used scRNA-seq to make the chromatin analysis of luteal endometrial tissue to identify candidate genes, which specifically expressed in endometrial epithelial cells in patients with RIF.