Macrophages: emerging targets for ulcerative colitis.

IF 5.9 2区医学 Q1 IMMUNOLOGY

Frontiers in Immunology Pub Date : 2025-09-15 eCollection Date: 2025-01-01 DOI:10.3389/fimmu.2025.1623491

Siqing Chen, Zhang Qin, Xiaoyuan Lin, Sainan Zhou, Yin Xu, Ying Zhu

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引用次数: 0

Abstract

Background: Ulcerative colitis (UC) is a chronic inflammatory bowel (IBD) disease characterized by a complex pathogenesis and limited treatment options. Macrophages play a key role in the pathophysiology of UC by regulating inflammatory responses and tissue repair processes. Currently, there is no comprehensive summary of macrophage regulatory pathways in UC, either domestically or internationally.

Objective: This review aims to systematically elucidate the role of macrophages in UC and their specific regulatory mechanisms, and to identify potential therapeutic strategies and future research directions.

Methods: A comprehensive literature review was conducted, integrating recent advances from global studies to explore macrophage-related pathways and functional alterations in UC. Special attention was given to studies investigating molecular mechanisms underlying macrophage polarization and function.

Results: Evidence indicates that macrophage dysfunction is a central mechanism in the pathogenesis of UC. Major findings demonstrate that metabolic reprogramming serves as a fundamental pathway inducing phenotypic and functional alterations in macrophages. Additional mechanisms mediating these changes include epigenetic modifications, chemokine-driven recruitment, microbial metabolite induction, autophagy, and apoptosis. Multiple drugs targeting macrophages have shown effectiveness in treating UC.

Conclusion: Targeting macrophage-related pathways represents an effective therapeutic approach for UC. This review provides a theoretical foundation for developing precision treatments focused on macrophage modulation and highlights important new avenues for future research.

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巨噬细胞：溃疡性结肠炎的新靶点。

背景：溃疡性结肠炎（UC）是一种慢性炎症性肠（IBD）疾病，其发病机制复杂，治疗方案有限。巨噬细胞通过调节炎症反应和组织修复过程在UC的病理生理中发挥关键作用。目前，无论是国内还是国际上都没有对UC中巨噬细胞的调控途径进行全面的总结。目的：本综述旨在系统阐明巨噬细胞在UC中的作用及其具体调控机制，并确定潜在的治疗策略和未来的研究方向。方法：进行全面的文献综述，整合全球研究的最新进展，探索UC中巨噬细胞相关途径和功能改变。特别关注巨噬细胞极化和功能的分子机制研究。结果：有证据表明巨噬细胞功能障碍是UC发病的中心机制。主要研究结果表明，代谢重编程是诱导巨噬细胞表型和功能改变的基本途径。介导这些变化的其他机制包括表观遗传修饰、趋化因子驱动的募集、微生物代谢物诱导、自噬和细胞凋亡。针对巨噬细胞的多种药物已显示出治疗UC的有效性。结论：靶向巨噬细胞相关通路是治疗UC的有效途径。本文综述为巨噬细胞调控的精准治疗提供了理论基础，并为今后的研究提供了重要的新途径。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Frontiers in Immunology IMMUNOLOGY-

CiteScore

9.80

自引率

11.00%

发文量

7153

审稿时长

14 weeks

期刊介绍： Frontiers in Immunology is a leading journal in its field, publishing rigorously peer-reviewed research across basic, translational and clinical immunology. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide. Frontiers in Immunology is the official Journal of the International Union of Immunological Societies (IUIS). Encompassing the entire field of Immunology, this journal welcomes papers that investigate basic mechanisms of immune system development and function, with a particular emphasis given to the description of the clinical and immunological phenotype of human immune disorders, and on the definition of their molecular basis.