| 项目编号 |
PRJCA036079 |
| 项目标题 |
Maternal causation of early-onset pre-eclampsia: excessive endometrial gland-derived apolipoprotein D induces placental ferroptosis and developmental abnormalities |
| 涉及领域 |
Medical |
| 数据类型 |
Biomarkers
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| 物种名称 |
Homo sapiens
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| 描述信息 |
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. Our study provides the first direct evidence that dysregulated endometrial gland function causes defective placental development and ePE, identifying APOD as a potential target for early diagnosis and therapeutic intervention. |
| 样品范围 |
Monoisolate |
| 发布日期 |
2025-02-13 |
| 项目资金来源 |
| 机构 |
项目类型 |
授权项目ID |
授权项目名称 |
| No funding support
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| 提交者 |
Dandan
Cao (sd2010bioinfo@gmail.com)
|
| 提交单位 |
The University of Hong Kong-Shenzhen Hospital |
| 提交日期 |
2025-02-13 |
