上海交通大学学报（医学版）

上海交通大学学报（医学版） >

2026 , Vol. 46 >Issue 4: 537 - 544

DOI: https://doi.org/10.3969/j.issn.1674-8115.2026.04.014

综述

巨噬细胞代谢重编程在复发性流产中的作用综述

  • 杜鑫 ,
  • 李雪冰 ,
  • 李永伟
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  • 1.河南中医药大学第二临床医学院，郑州 450002
    2.河南省中医院，郑州 450002
李永伟，主任技师，博士；电子信箱：lyw@hactcm.edu.cn。

收稿日期: 2025-07-29

  录用日期: 2025-10-23

  网络出版日期: 2026-04-10

基金资助

河南省高等学校重点科研项目(24A320007)

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Research progress of macrophage metabolic reprogramming in recurrent spontaneous abortion

  • Du Xin ,
  • Li Xuebing ,
  • Li Yongwei
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  • 1.Second Clinical Medical College, Henan University of Chinese Medicine, Zhengzhou 450002, China
    2.Henan Province Hospital of Traditional Chinese Medicine, Zhengzhou 450002, China
Li Yongwei, E-mail: lyw@hactcm.edu.cn.

Received date: 2025-07-29

  Accepted date: 2025-10-23

  Online published: 2026-04-10

Supported by

Key Research Project of Henan Province Universities(24A320007)

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摘要

复发性流产发病过程复杂，涉及多种免疫和代谢因素，具体机制尚不清楚。近年来，巨噬细胞通过代谢途径影响胚胎着床和维持妊娠稳定性的作用逐渐受到关注。巨噬细胞代谢主要包括糖代谢、脂代谢和氨基酸代谢。糖代谢主要通过影响糖酵解导致M1巨噬细胞极化，脂肪酸氧化减少与巨噬细胞抗炎功能受损相关，胆固醇积累加剧局部炎症反应，脂类代谢失衡也可影响蜕膜血管生成及胎盘发育。目前，研究已证实蜕膜局部微环境的代谢紊乱如缺氧和氧化应激，可直接诱导巨噬细胞发生代谢重编程，进而影响其促炎或抗炎作用转换；但巨噬细胞代谢关键节点在妊娠免疫调控中的具体作用机制，以及靶向代谢途径干预的可行性，仍需深入探讨。该文总结巨噬细胞在复发性流产中的作用，并聚焦于代谢重编程这一核心调控节点，深入探讨糖代谢、脂代谢及氨基酸代谢失衡如何驱动巨噬细胞功能紊乱，进而影响母胎界面免疫耐受微环境的建立与维持，为复发性流产的防治研究提供新的视角。

关键词： 复发性流产; 巨噬细胞; 代谢途径; 胚胎着床; 妊娠稳定性

本文引用格式

杜鑫 , 李雪冰 , 李永伟 . 巨噬细胞代谢重编程在复发性流产中的作用综述[J]. 上海交通大学学报（医学版）, 2026 , 46(4) : 537 -544 . DOI: 10.3969/j.issn.1674-8115.2026.04.014

Abstract

The mechanisms underlying recurrent spontaneous abortion (RSA) remain unclear, as its pathogenesis is complex and involves multiple immune and metabolic factors. In recent years, increasing attention has been directed toward the mechanisms by which macrophages influence embryo implantation and pregnancy maintenance through metabolic pathways. Macrophage metabolism primarily encompasses glucose metabolism, lipid metabolism, and amino acid metabolism. Glucose metabolism drives M1 macrophage polarization primarily through glycolysis, while reduced fatty acid oxidation is associated with impaired anti-inflammatory functions of macrophages. Cholesterol accumulation exacerbates local inflammatory responses, and lipid metabolism imbalances may also affect decidual angiogenesis and placental development. Current research has confirmed that metabolic disturbances in the local decidual microenvironment, such as hypoxia and oxidative stress, can directly induce metabolic reprogramming of macrophages, subsequently affecting their pro-inflammatory or anti-inflammatory conversion. However, the specific mechanisms of key metabolic nodes of macrophages of pregnancy immune regulation, as well as the feasibility of targeted intervention through metabolic pathways, still require further investigation. This article reviews the role of macrophages in recurrent spontaneous abortion, focusing on metabolic reprogramming as a core regulatory node. It delves into how imbalances in glucose, lipid, and amino acid metabolism drive macrophage dysfunction, thereby affecting the establishment and maintenance of the immune-tolerant microenvironment at the maternal-fetal interface, aiming to provide new perspectives for the prevention and treatment of RSA.

Key words： recurrent spontaneous abortion; macrophages; metabolic pathways; embryo implantation; pregnancy stability

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