| Title |
Maternal causation of early-onset pre-eclampsia: excessive endometrial gland-derived apolipoprotein D induces placental ferroptosis and developmental abnormalities |
| Description |
Dysregulated secretory function of endometrial glands is suspected to impair placental development, though direct evidence has been lacking. Early-onset preeclampsia (ePE) is characterized by poor remodeling of maternal spiral arteries by extravillous trophoblasts (EVTs), a key step in placental development. By analyzing endometrial glandular organoids from ePE and normotensive pregnancies, we found elevated APOD levels in ePE samples. Overexpression of endometrial APOD impaired EVT and endothelial cell vascular remodeling functions in vitro. These findings were further validated using an endometrial-specific APOD knock-in mouse model. APOD triggered ferroptosis through the PI3K/Akt pathway in both human ePE placentas and the mouse model. Elevated APOD levels in first-trimester serum samples from women who later developed ePE suggest its potential as an early biomarker. |
| Organism |
Homo sapiens |
| Data Type |
Other Type of Image Data |
| Data Accessibility |
Controlled-access |
| BioProject |
PRJCA036246 |
| Release Date |
2026-01-03 |
| Submitter |
Zhao Zhiang (pchiucn@hku-szh.org) |
| Organization |
The University of Hong Kong—Shenzhen Hospital |
| Submission Date |
2025-02-17 |