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脓毒症中的巨噬细胞极化:新出现的作用及临床应用前景

Macrophage polarization in sepsis: Emerging role and clinical application prospect.

作者信息

Hou Fei Fei, Mi Jun Hao, Wang Qiong, Tao Yan Lin, Guo Shuai Bin, Ran Guang He, Wang Jing Chao

机构信息

Intensive Care Unit Inner Mongolia Medical University Affiliated Hospital, Hohhot 010050, China.

Liuzhou Maternity and Child Healthcare Hospital, Liuzhou 545001, China.

出版信息

Int Immunopharmacol. 2025 Jan 10;144:113715. doi: 10.1016/j.intimp.2024.113715. Epub 2024 Dec 3.

DOI:10.1016/j.intimp.2024.113715
PMID:39626538
Abstract

Sepsis is a severe, potentially fatal condition defined by organ dysfunction due to excessive inflammation. Its complex pathogenesis and poor therapeutic outcomes pose significant challenges in treatment. Macrophages, with their high heterogeneity and plasticity, play crucial roles in both the innate and adaptive immune systems. They can polarize into M1-like macrophages, which promote pro-inflammatory responses, or M2-like macrophages, which mediate anti-inflammatory responses, positioning them as critical mediators in the immune response during sepsis.Macrophages are the main regulators of inflammatory responses, and their polarization is also regulated by inflammatory signaling pathways. This review highlights recent advances in the inflammatory signaling pathways involved in sepsis, mechanism of macrophage polarization mediated by inflammation-related signaling pathways in sepsis, and the role of signaling pathway mediated macrophage polarization in organ dysfunction involved in sepsis. We also explore the therapeutic potential of targeting macrophage polarization for immunotherapy, offering new perspectives on macrophage-targeted treatments for sepsis.

摘要

脓毒症是一种严重的、可能致命的疾病,其定义为由于过度炎症导致的器官功能障碍。其复杂的发病机制和较差的治疗效果给治疗带来了重大挑战。巨噬细胞具有高度的异质性和可塑性,在固有免疫系统和适应性免疫系统中均发挥着关键作用。它们可以极化为促进促炎反应的M1样巨噬细胞,或介导抗炎反应的M2样巨噬细胞,这使它们成为脓毒症免疫反应中的关键介质。巨噬细胞是炎症反应的主要调节因子,其极化也受炎症信号通路的调控。本综述重点介绍了脓毒症相关炎症信号通路的最新进展、脓毒症中炎症相关信号通路介导巨噬细胞极化的机制,以及信号通路介导的巨噬细胞极化在脓毒症相关器官功能障碍中的作用。我们还探讨了针对巨噬细胞极化进行免疫治疗的潜在治疗价值,为脓毒症的巨噬细胞靶向治疗提供了新的视角。

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引用本文的文献

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Burns Trauma. 2025 Jul 15;13:tkaf046. doi: 10.1093/burnst/tkaf046. eCollection 2025.
2
FGF15/FGFR4 signaling suppresses M1 macrophage polarization and multi-organ inflammation in septic mice by inhibiting H3K18 lactylation-driven Irf7 expression through NF2-Hippo activation.成纤维细胞生长因子15/成纤维细胞生长因子受体4信号通路通过激活NF2-河马通路抑制H3K18乳酸化驱动的干扰素调节因子7表达,从而抑制脓毒症小鼠的M1巨噬细胞极化和多器官炎症。
Cell Death Dis. 2025 Aug 19;16(1):628. doi: 10.1038/s41419-025-07962-w.
3
Immunothrombosis in Sepsis: Cellular Crosstalk, Molecular Triggers, and Therapeutic Opportunities-A Review.
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Int J Mol Sci. 2025 Jun 25;26(13):6114. doi: 10.3390/ijms26136114.