国际妇产科学杂志 ›› 2025, Vol. 52 ›› Issue (6): 643-648.doi: 10.12280/gjfckx.20250733

• 产科生理及产科疾病:综述 • 上一篇    下一篇

蛋白质乳酸化修饰在胎盘缺氧及妊娠并发症中的研究进展

王军, 孙晓彤(), 蒲瑞阳, 张磊磊   

  1. 730000 兰州,甘肃中医药大学第一临床医学院(王军,张磊磊);甘肃省人民医院产科(孙晓彤,蒲瑞阳)
  • 收稿日期:2025-07-02 出版日期:2025-12-15 发布日期:2025-12-30
  • 通讯作者: 孙晓彤 E-mail:13919101217@163.com
  • 基金资助:
    甘肃省自然科学基金(24JRRA597);甘肃省人民医院院内科研基金(23GSSYD-1)

Research Progress on Protein Lactylation Modification in Placental Hypoxia and Pregnancy Complications

WANG Jun, SUN Xiao-tong(), PU Rui-yang, ZHANG Lei-lei   

  1. First School of Clinical Medical College, Gansu University of Chinese Medicine, Lanzhou 730000, China (WANG Jun, ZHANG Lei-lei); Department of Obstetrics, Gansu Provincial Hospital, Lanzhou 730000, China (SUN Xiao-tong, PU Rui-yang)
  • Received:2025-07-02 Published:2025-12-15 Online:2025-12-30
  • Contact: SUN Xiao-tong E-mail:13919101217@163.com

摘要:

乳酸累积介导的蛋白质乳酸化修饰是一种新的表观遗传修饰,是乳酰基与蛋白质赖氨酸残基共价偶联,从而调控基因表达的蛋白质修饰方式。由于妊娠早期的胎盘存在生理性缺氧,使得胎盘细胞产生了一系列缺氧反应机制,在这些缺氧反应机制中已发现不同程度的蛋白质乳酸化修饰的参与,蛋白质乳酸化修饰介导细胞能量流向、滋养细胞功能表达、免疫功能和炎症反应等。当胎盘出现病理性缺氧时会导致胎盘功能障碍、异常滋养细胞增殖和侵袭功能受损,并在此基础上发生子痫前期(preeclampsia,PE)、妊娠期糖尿病(gestational diabetes mellitus,GDM)和复发性流产(recurrent spontaneous abortion,RSA)等妊娠并发症,PE和GDM患者中高表达的蛋白乳酸化水平会导致胎盘功能障碍,降低滋养细胞迁移和侵袭能力,参与疾病的发生发展;蛋白质乳酸化修饰通过调控滋养细胞凋亡和母胎界面免疫参与RSA发病。综述蛋白质乳酸化修饰在胎盘缺氧及妊娠并发症中的研究进展,为胎盘源性胎儿缺氧相关妊娠并发症的预防和治疗提供新思路。

关键词: 蛋白质加工,转译后, 胎盘, 低氧, 妊娠并发症, 乳酸化修饰

Abstract:

Protein lactylation modification mediated by lactate accumulation is a new type of epigenetic modification. It is a protein modification method in which lactyl groups are covalently coupled to lysine residues of proteins to regulate gene expression. Due to the physiological hypoxia in the placenta during early pregnancy, placental cells have developed a series of hypoxia-response mechanisms. Different degrees of protein lactylation modification have been found to be involved in these mechanisms. Protein lactylation modification mediates cellular energy flow, trophoblast cell function expression, immune function, and inflammatory responses. When pathological hypoxia occurs in the placenta, it can lead to placental dysfunction, abnormal trophoblast cell proliferation, and impaired invasion function. On this basis, pregnancy complications such as preeclampsia (PE), gestational diabetes mellitus (GDM), and recurrent spontaneous abortion (RSA) may occur. High levels of protein lactylation in patients with PE and GDM can cause placental dysfunction, reduce the migration and invasion ability of trophoblast cells, and participate in the occurrence and development of the diseases. Protein lactylation modification participates in the pathogenesis of RSA by regulating trophoblast cell apoptosis and the immune function at the maternal-fetal interface. This review summarizes the research progress of protein lactylation modification in placental hypoxia and pregnancy complications, aiming to provide new ideas for the prevention and treatment of placental-derived pregnancy complications related to fetal hypoxia.

Key words: Protein processing, post-translational, Placenta, Hypoxia, Pregnancy complications, Lactylation