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妊娠期缺氧所致线粒体/内质网应激在子痫前期/胎儿宫内生长受限中作用的研究进展

刘会芳^1,2,3,4, 格日力^1,2,3, 乌仁塔娜^1,2,3,*

¹青海大学高原医学研究中心高原医学教育部重点实验室，西宁 810001；² 青海省高原医学应用基础重点实验室，西宁 810001；³青海-犹他高原医学联合重点实验室，西宁 810001；⁴ 青海大学附属医院，西宁 810001

摘要

子痫前期和胎儿宫内生长受限(intrauterine growth restriction, IUGR)是世界范围内最常见的两种妊娠并发症，影响5%~10%的妊娠女性。子痫前期与孕产妇和胎儿的发病率及死亡率明显升高有关。缺氧引起的子宫胎盘功能障碍是子痫前期和IUGR的关键病理因素。氧气供应减少会破坏线粒体和内质网功能，低氧已被证明会改变线粒体活性氧的稳态，并诱发内质网应激。妊娠期缺氧与胎盘中活性氧的过度产生有关，导致氧化应激，氧化应激在包括妊娠期高血压在内的许多人类疾病中都有发生，研究表明，子痫前期和IUGR的子宫胎盘组织/细胞显示出较高水平的氧化应激，在这两种并发症的发病机制中起着重要作用。本综述总结了缺氧导致线粒体氧化应激/内质网应激在子痫前期/IUGR发病机制中的作用，并讨论了靶向氧化应激的潜在治疗策略，为治疗这两种妊娠并发症提供参考。

关键词： 缺氧; 子痫前期; 胎儿宫内生长受限; 线粒体; 内质网

Research progress on the effect of mitochondrial and endoplasmic reticulum stress caused by hypoxia during pregnancy on preeclampsia and intrauterine growth restriction 

LIU Hui-Fang^1,2,3,4, GE Ri-Li^1,2,3, WUREN Ta-Na^1,2,3,*

¹Key Laboratory of Plateau Medicine of Ministry of Education, Plateau Medicine Research Center, Qinghai University, Xining 810001, China ；²Qinghai Key Laboratory of Plateau Medicine Application Foundation, Xining 810001, China ；³Qinghai-Utah Joint Key Laboratory of Plateau Medicine, Xining 810001, China；⁴Affiliated Hospital of Qinghai University, Xining 810001, China

Abstract

Preeclampsia and intrauterine growth restriction (IUGR) of the fetus are the two most common pregnancy complications worldwide, affecting 5%–10% of pregnant women. Preeclampsia is associated with significantly increased maternal and fetal morbidity and mortality. Hypoxia-induced uteroplacental dysfunction is now recognized as a key pathological factor in preeclampsia and IUGR. Reduced oxygen supply (hypoxia) disrupts mitochondrial and endoplasmic reticulum (ER) function. Hypoxia has been shown to alter mitochondrial reactive oxygen species (ROS) homeostasis and induce ER stress. Hypoxia during pregnancy is associated with excessive production of ROS in the placenta, leading to oxidative stress. Oxidative stress occurs in a number of human diseases, including high blood pressure during pregnancy. Studies have shown that uterine placental tissue/cells in preeclampsia and IUGR show high levels of oxidative stress, which plays an important role in the pathogenesis of both the complications. This review summarizes the role of hypoxia-induced mitochondrial oxidative stress and ER stress in the pathogenesis of preeclampsia/IUGR and discusses the potential therapeutic strategies targeting oxidative stress to treat both the pregnancy complications.

Key words: Hypoxia; preeclampsia; intrauterine growth restriction; mitochondrion; endoplasmic reticulum

收稿日期：　　录用日期：

通讯作者：乌仁塔娜　　E-mail: tanna.mgl@gmail.com

DOI: 10.13294/j.aps.2023.0060

引用本文：

刘会芳, 格日力, 乌仁塔娜. 妊娠期缺氧所致线粒体/内质网应激在子痫前期/胎儿宫内生长受限中作用的研究进展[J]. 生理学报 2023; 75 (5): 714-726.

LIU Hui-Fang, GE Ri-Li, WUREN Ta-Na. Research progress on the effect of mitochondrial and endoplasmic reticulum stress caused by hypoxia during pregnancy on preeclampsia and intrauterine growth restriction . Acta Physiol Sin 2023; 75 (5): 714-726 (in Chinese with English abstract).