高迁移率族蛋白A2在胎儿生长受限发病机制中的研究进展  

Advances in the Pathogenesis of Fetal Growth Restriction by HMGA2

作　　者：侯春艳 杜秀萍(审校)[1] 王红红[1] 侯岳洋 HOU Chun-yan;DU Xiu-ping;WANG Hong-hong;HOU Yue-yang(Clinical Discipline Construction Center,Shanxi Medical University,Taiyuan 030000,China)

机构地区：[1]山西医科大学临床学科建设中心,太原030000

出　　处：《国际妇产科学杂志》2025年第2期127-131,共5页Journal of International Obstetrics and Gynecology

摘　　要：胎儿生长受限(fetal growth restriction,FGR)是导致死胎和新生儿不良结局的主要妊娠并发症之一,其发病机制复杂且临床治疗手段有限。高迁移率族蛋白A2(high-mobility group protein A2,HMGA2)作为一种非组蛋白染色质蛋白,在胚胎发育、血管生成及细胞凋亡调控中发挥关键作用。近年研究表明,HMGA2通过调节血管生成、内皮细胞功能及多器官发育相关信号通路,可能参与FGR的病理过程。综述HMGA2在FGR发病机制中的研究进展,探讨其在胎盘功能、胎儿缺氧耐受及器官发育中的潜在作用,旨在为FGR的早期预测、诊断及靶向治疗提供新的理论依据和干预策略。深入研究HMGA2的功能及其调控网络,不仅有助于揭示FGR的分子机制,也为未来开发精准医疗方案奠定了重要基础。Fetal growth restriction(FGR)is one of the major pregnancy complications leading to stillbirth and adverse outcomes in newborns,with complex pathogenesis and limited clinical treatment.High-mobility group protein A2(HMGA2),a non-histone chromatin protein,plays a key role in embryonic development,angiogenesis and apoptosis regulation.Recent studies have shown that HMGA2 may be involved in the pathological process of FGR by regulating angiogenesis,endothelial cell function and multi-organ development-related signalling pathways.This article reviews the research progress of HMGA2 in the pathogenesis of FGR and explores its potential role in placental function,foetal hypoxia tolerance and organ development,with aim of providing a new theoretical basis and intervention strategy for the early prediction,diagnosis and targeted treatment of FGR.The in-depth study of the function of HMGA2 and its regulatory network will not only helps to reveal the molecular mechanism of FGR,but also lays an important foundation for the development of precision medicine therapeutic solutions in the future.

关 键 词：胎儿生长迟缓 胎儿发育 HMGA2蛋白 信号传导 血管内皮生长因子类 

分 类 号：R714.5[医药卫生—妇产科学]