综述

2型糖尿病创面愈合中巨噬细胞代谢调控的研究进展

  • 黄英荷 ,
  • 招冠钰 ,
  • 孙阳 ,
  • 侯鉴基 ,
  • 左勇
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  • 1.广东医科大学海洋医药研究院,湛江 524023
    2.上海交通大学基础医学院生物化学与分子细胞生物学系,上海 200025
黄英荷(2001—),女,硕士生;电子信箱:1152451431@qq.com
第一联系人:黄英荷负责确定文章选题、结构,文献收集,写作及修改工作;招冠钰参与文章选题、文献收集和修改;孙阳、侯鉴基参与文章修改;左勇负责写作指导和修改。所有作者均阅读并同意了最终稿件提交。
左 勇,研究员,博士;电子信箱:zuoyong@shsmu.edu.cn

收稿日期: 2025-02-24

  录用日期: 2025-03-26

  网络出版日期: 2025-06-23

基金资助

国家自然科学基金(81870321)

Research progress on macrophage metabolic regulation in wound healing of diabetes mellitus type 2

  • HUANG Yinghe ,
  • ZHAO Guanyu ,
  • SUN Yang ,
  • HOU Jianji ,
  • ZUO Yong
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  • 1.Marine Biomedical Research Institute, Guangdong Medical University, Zhanjiang 524023, China
    2.Department of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University College of Basic Medical Sciences, Shanghai 200025, China
First author contact:HUANG Yinghe was responsible for determining the topic and structure, collecting literature, and writing and revising the manuscript. ZHAO Guanyu participated in the topic selection, literature collection, and revision of the manuscript. SUN Yang and HOU Jianji participated in the revision of the manuscript. ZUO Yong was responsible for writing guidance and revision. All authors have read the final version of the paper and consented to its submission.
ZUO Yong, E-mail: zuoyong@shsmu.edu.cn.

Received date: 2025-02-24

  Accepted date: 2025-03-26

  Online published: 2025-06-23

Supported by

National Natural Science Foundation of China(81870321)

摘要

全球成人糖尿病患病率逐年递增,其中以2型糖尿病(diabetes mellitus type 2,T2DM)为主。T2DM是由胰岛素抵抗和胰岛素分泌不足引起的伴随糖、蛋白质和脂肪代谢紊乱的一种慢性疾病。创面愈合障碍是T2DM的主要并发症之一。研究表明T2DM患者创面愈合受巨噬细胞调控,并与其表型、活性和数量相关。不同表型的巨噬细胞在T2DM创面愈合的各个阶段扮演不同角色:M1型巨噬细胞参与创伤早期的炎症反应和病原体清除,M2型巨噬细胞在创面愈合后期发挥抗炎症作用并介导创面修复。巨噬细胞表型转换障碍影响创面炎症反应、皮肤细胞功能和细胞外基质(extracellular matrix,ECM)合成等过程,最终导致愈合障碍。目前,巨噬细胞代谢改变与表型转换之间的相互作用机制研究取得了显著进展,且这种动态关联可能通过协同调控参与T2DM创面的愈合进程。该文总结巨噬细胞在正常创面愈合与T2DM患者创面愈合中的功能特点,就病理环境下巨噬细胞糖代谢、脂质代谢和氨基酸代谢变化及这些变化对创面愈合的调控作用展开综述,并讨论靶向巨噬细胞代谢治疗创面愈合的应用前景。

本文引用格式

黄英荷 , 招冠钰 , 孙阳 , 侯鉴基 , 左勇 . 2型糖尿病创面愈合中巨噬细胞代谢调控的研究进展[J]. 上海交通大学学报(医学版), 2025 , 45(6) : 792 -799 . DOI: 10.3969/j.issn.1674-8115.2025.06.015

Abstract

The global prevalence of diabetes among adults is increasing year by year, with diabetes mellitus type 2 (T2DM) being the most common form. T2DM is a chronic disease characterized by insulin resistance and insufficient insulin secretion, often accompanied by disturbances in glucose, protein, and lipid metabolism. Impaired wound healing is one of the major complications of T2DM. Studies have shown that wound healing in T2DM patients are regulated by macrophages and are closely related to their phenotype, activity, and abundance. Macrophages of different phenotypes play distinct roles in various stages of T2DM wound healing: M1 macrophages are involved in the early inflammatory response and pathogen clearance, while M2 macrophages contribute to anti-inflammatory responses and wound repair during later stages. Dysregulation of macrophage phenotype switching affects wound inflammatory response, skin cell function, and extracellular matrix (ECM) synthesis, ultimately leading to impaired healing. Significant progress has been made in understanding the interactions between macrophage metabolic changes and phenotype switching, and this dynamic relationship might play a synergistic role in regulating the wound healing process in T2DM. This review summarizes the functional roles of macrophages in both normal and T2DM-associated wound healing, discusses alterations in glucose, lipid, and amino acid metabolism in macrophages under pathological conditions, and explores how these metabolic shifts regulate wound healing. Furthermore, it examines the therapeutic potential of targeting macrophage metabolism to improve wound healing outcomes.

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