Dysregulated placental autophagy and preeclampsia
10.3760/cma.j.cn113903-20250227-00091
- VernacularTitle:胎盘自噬异常与子痫前期
- Author:
Weichen PAN
1
;
Huaijun FEI
;
Guangfeng ZHAO
;
Mingming ZHENG
Author Information
1. 南京医科大学鼓楼临床医学院，南京 210008
- Publication Type:Journal Article
- Keywords:
Autophagy;
Preeclampsia;
Trophoblast;
Immune cell
- From:
Chinese Journal of Perinatal Medicine
2025;28(7):615-618
- CountryChina
- Language:Chinese
-
Abstract:
Preeclampsia is a placenta-originated disorder closely associated with impaired placental development and immune imbalance at the maternal-fetal interface. As a critical process in the regulation of cellular homeostasis, autophagy plays a pivotal role in trophoblast syncytialization, invasion, and immune tolerance at the maternal-fetal interface. Moderate autophagy enhances trophoblast function and promotes spiral artery remodeling, whereas insufficient or excessive autophagy correlates with placental pathological features of preeclampsia, including impaired syncytialization, protein aggregate accumulation, and immune dysregulation. Although trophoblast-specific autophagy deficiencies in animal models can manifest preeclampsia-like phenotypes, clinical studies reveal tissue-specific variability in autophagy-related protein expression, which may be attributable to placental regional heterogeneity, disease subtypes, and sampling timepoints. Future investigations integrating multi-stage clinical cohorts, multicellular models, and genetically modified animals are warranted to elucidate the dynamic role of autophagy in preeclampsia pathogenesis and establish its causal relationship with disease progression, thereby providing a basis for targeted therapeutic strategies.
