国际妇产科学杂志 ›› 2025, Vol. 52 ›› Issue (4): 366-370.doi: 10.12280/gjfckx.20250297

• 产科生理及产科疾病:综述 • 上一篇    下一篇

自噬在子痫前期发病中的作用机制及相关治疗进展

杨瑶瑶, 王永红()   

  1. 030001 太原,山西医科大学第二医院妇产科
  • 收稿日期:2025-03-24 出版日期:2025-08-15 发布日期:2025-09-08
  • 通讯作者: 王永红,E-mail:wangyh19672000@126.com
  • 作者简介:审校者
  • 基金资助:
    山西省自然科学基金面上项目(202403021211166)

Research Progress on the Mechanism of Autophagy in the Pathogenesis of Preeclampsia and Related Treatments

YANG Yao-yao, WANG Yong-hong()   

  1. Department of Obstetrics and Gynecology, Second Hospital of Shanxi Medical University, Taiyuan 030001, China
  • Received:2025-03-24 Published:2025-08-15 Online:2025-09-08
  • Contact: WANG Yong-hong, E-mail: wangyh19672000@126.com

摘要:

子痫前期(preeclampsia,PE)是一种妊娠期特有的多系统功能障碍性疾病,其特征为妊娠20周后新发高血压、蛋白尿等,严重时可进展为子痫,是全球范围内孕产妇和新生儿预后不良甚至死亡的重要原因之一。PE发病机制复杂,涉及胎盘发育异常、血管内皮功能障碍、氧化应激失衡等多种病理生理过程。近年研究发现,自噬作为细胞重要的稳态调控机制,通过溶酶体途径降解受损细胞器、错误折叠蛋白,在PE发生发展中发挥关键作用。具体而言,自噬通过调控滋养细胞侵袭能力、子宫螺旋动脉重塑过程、氧化应激水平、炎症反应强度以及内质网应激状态等多个环节参与PE的病理进程。值得注意的是,多种信号分子和药物可通过调节自噬活性影响PE的疾病进展,为开发新型靶向治疗策略提供了理论依据。综述自噬在PE发病机制中的分子作用及其治疗潜力,旨在为深入理解PE的病理机制和临床防治提供新视角。

关键词: 先兆子痫, 自噬, 内质网应激, 氧化性应激, 血管生成

Abstract:

Preeclampsia (PE) is a pregnancy-specific multisystem dysfunction disorder characterized by newly developed hypertension and proteinuria after 20 weeks of gestation. In severe cases, it can progress to eclampsia, which remains one of the important causes of poor prognosis and mortality for pregnant women and newborns globally. The pathogenesis of PE is complex, involving multiple pathophysiological processes such as abnormal placental development, vascular endothelial dysfunction, and oxidative stress imbalance. In recent years, studies have found that autophagy, an essential cellular homeostasis regulatory mechanism, degrades organelles and misfolded proteins through the lysosomal pathway and plays a key role in the occurrence and development of PE. Specifically, autophagy participates in the pathological process of PE by regulating multiple aspects, including the invasive ability of trophoblasts, the remodeling process of uterine spiral arteries, and the level of oxidative stress, the intensity of inflammatory response, and the state of endoplasmic reticulum stress. Notably, various signaling molecules and drugs can affect the progression of PE by regulating autophagy activity, providing a theoretical basis for the development of novel targeted therapeutic strategies. This review summarizes the molecular role of autophagy in the pathogenesis of PE and its therapeutic potential, aiming to provide new perspectives for a deeper understanding of the pathological mechanisms and its clinical prevention and treatment.

Key words: Pre-eclampsia, Autophagy, Endoplasmic reticulum stress, Oxidative stress, Angiogenesis