SHP2 improved Late-onset fetal growth restriction via modulating ROS/BRD4/PI3K/YAP/PIGF signaling induced angiogenesis.

ABSTRACT:

Objective

To look into the molecular processes and function of SHP2 in late-onset fetal growth restriction (LO-FGR).

Methods

An elaborate research technique included in vitro experiments and bioinformatics analysis. By identifying differentially expressed genes (DEGs) and enriched pathways linked to fetal growth restriction (FGR), the bioinformatics analysis of the GSE147776 dataset offered first insights into putative signaling networks, such as angiogenesis and oxidative stress. This bioinformatic information served as a guide for in vitro investigations using endothelial progenitor cells (EPCs) grown under circumstances similar to LO-FGR. EPCs were divided into six groups based on different drug treatments: NC group, Model group, Model + JQ-1 group, Model + JQ-1 + PHPS1 g

SUBMITTER: Li F 

PROVIDER: S-EPMC12904435 | biostudies-literature | 2026

REPOSITORIES: biostudies-literature