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

doi:10.12280/gjfckx.20250297

Abstract

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

YANG Yao-yao, WANG Yong-hong. Research Progress on the Mechanism of Autophagy in the Pathogenesis of Preeclampsia and Related Treatments[J]. Journal of International Obstetrics and Gynecology, 2025, 52(4): 366-370.

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