Shuyun Li

Impact of vitamin D deficiency on defective endometrial decidualization and the repressive role of vitamin D receptor (VDR) in the epigenomic network

This study shows that vitamin D receptor (VDR) regulates endometrial decidualization by modulating chromatin accessibility and gene expression, with implications for fertility and uterine disorders.

Macrophages regulate meiotic initiation and germ cell clearance in the developing ovary

This study shows ovarian macrophages regulate germ cell meiotic entry, vascular growth, and germ cell clearance during oocyte reserve establishment.

Prenatal corticosteroid exposure disrupts vascular-immune interactions and impairs steroidogenesis in the fetal testis

Prenatal corticosteroid exposure disrupts immune-vascular interactions and impairs steroidogenesis in the fetal testis, revealing potentially widespread effects of a commonly used therapy.

Deciphering ESR1-driven transcription in human endometrial stromal cells via transcriptome, cistrome, and integration with chromatin landscape

This study investigates ESR1 and estrogen-driven transcription in human endometrial stromal cells using transcriptome, cistrome, and chromatin landscape data to identify gene regulation and its implications in decidualization and endometrial cancer.

Testis morphogenesis and fetal Leydig cell development are mediated through ERK signaling activated by platelet derived growth factor receptor alpha

The paper investigates the role of PDGFRA and ERK signaling in fetal testis morphogenesis and Leydig cell development using genetic and molecular approaches.

Perivascular cells support folliculogenesis in the developing ovary

The paper identifies Nestin+ perivascular cells in mice as multipotent progenitors contributing to ovarian lineages and shows their role in folliculogenesis through Notch signaling.

Loss of Mafb and Maf distorts myeloid cell ratios and disrupts fetal mouse testis vascularization and organogenesis

The paper shows that deleting Mafb and Maf genes in fetal mouse gonads causes monocyte overproduction and defects in vascularization and testis development.