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中华损伤与修复杂志(电子版) ›› 2026, Vol. 21 ›› Issue (01) : 69 -74. doi: 10.3877/cma.j.issn.1673-9450.2026.01.012

综述

巨噬细胞代谢重编程在脓毒症急性肺损伤中作用的研究进展
何林霞1, 相阳2, 刘心如1, 郑兴锋2,()   
  1. 1 200444 上海大学转化医学研究院
    2 200438 上海,海军军医大学第一附属医院烧伤科
  • 收稿日期:2025-09-10 出版日期:2026-02-01
  • 通信作者: 郑兴锋
  • 基金资助:
    上海市自然科学基金(23ZR1478800)

Research progress on the role of macrophage metabolic reprogramming in sepsis-induced acute lung injury

Linxia He1, Yang Xiang2, Xinru Liu1, Xingfeng Zheng2,()   

  1. 1 Institute of Translational Medicine, Shanghai University, Shanghai 200444, China
    2 Department of Burn Surgery, the First Affiliated Hospital of Naval Medical University, Shanghai 200438, China
  • Received:2025-09-10 Published:2026-02-01
  • Corresponding author: Xingfeng Zheng
引用本文:

何林霞, 相阳, 刘心如, 郑兴锋. 巨噬细胞代谢重编程在脓毒症急性肺损伤中作用的研究进展[J/OL]. 中华损伤与修复杂志(电子版), 2026, 21(01): 69-74.

Linxia He, Yang Xiang, Xinru Liu, Xingfeng Zheng. Research progress on the role of macrophage metabolic reprogramming in sepsis-induced acute lung injury[J/OL]. Chinese Journal of Injury Repair and Wound Healing(Electronic Edition), 2026, 21(01): 69-74.

在脓毒症急性肺损伤中,巨噬细胞功能失调是炎症失控和组织损伤的关键。代谢重编程是连接脓毒症微环境与巨噬细胞功能失调的核心机制。脓毒症急性肺损伤微环境可诱导巨噬细胞的糖、脂、氨基酸代谢及线粒体功能等方面发生显著的代谢重编程,这些改变驱动巨噬细胞过度激活促炎反应,抑制其抗炎与组织修复功能,从而加剧肺损伤。靶向代谢重编程的治疗策略虽具有抗炎与组织保护潜力,但仍面临巨噬细胞异质性、代谢网络复杂性及临床转化等挑战。未来需深入解析不同巨噬细胞亚群的代谢特征,开发精准干预手段,并探索代谢重编程作为预后标志物的潜力,以期为改善脓毒症急性肺损伤预后提供新途径。

Macrophage dysfunction is a key factor in uncontrolled inflammation and tissue injury in sepsis-induced acute lung injury. Metabolic reprogramming serves as a critical bridge linking the septic microenvironment to macrophage dysfunction. During sepsis-induced acute lung injury, macrophages undergo significant reprogramming in glucose metabolism, lipid metabolism, amino acid metabolism, and mitochondrial function. These metabolic alterations drive hyperactivation of pro-inflammatory responses while suppressing anti-inflammatory and tissue-repair functions, ultimately exacerbating lung injury. Therapeutic strategies targeting metabolic reprogramming may be beneficial for anti-inflammatory and tissue-protection, but face challenges of macrophage heterogeneity, metabolic network complexity, and clinical translation barriers. Future research requires in-depth analysis of metabolic signatures across distinct macrophage subsets, development of precise interventions, and exploration of metabolic reprogramming as a prognostic biomarker. This approach may facilitate the emergence of targeted metabolic reprogramming as a novel pathway to improve outcomes in sepsis-induced acute lung injury.

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