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巨噬细胞代谢重编程调控慢加急性肝衰竭的机制与治疗前景

肖滢 马路园 董世龙 王亚东 赵彩彦

引用本文:
Citation:

巨噬细胞代谢重编程调控慢加急性肝衰竭的机制与治疗前景

DOI: 10.12449/JCH251230
基金项目: 

中央引导地方科技发展资金项目(科技创新基地建设) (236Z7749G);

河北省研究生创新资助项目 (CXZZBS2026110)

利益冲突声明:本文不存在任何利益冲突。
作者贡献声明:肖滢负责查阅文献,撰写文章;马路园、董世龙负责文章修改;王亚东、赵彩彦负责指导立题,文章审校与修改。
详细信息
    通信作者:

    赵彩彦, zhaocy@hebmu.edu.cn (ORCID: 0000-0001-5997-4641)

Mechanism and treatment prospects of macrophage metabolic reprogramming in regulating acute-on-chronic liver failure

Research funding: 

Central Guiding Local Technology Development Fund Project (Construction of Science and Technology Innovation Base) (236Z7749G);

Hebei Province Graduate Innovation Funding Project (CXZZBS2026110)

More Information
  • 摘要: 代谢重编程是巨噬细胞表型转变的前提和重要标志,不同巨噬细胞表型通过调节炎症反应平衡参与慢加急性肝衰竭(ACLF)发病机制,因此成为ACLF治疗潜在靶位。本综述重点关注ACLF进程中巨噬细胞代谢重编程的变化规律,以及其通过调控能量代谢与免疫炎症介导ACLF严重程度和预后转归的机制,为开发基于巨噬细胞代谢重编程为靶位的ACLF防治策略提供新的思路和方向。

     

  • 注: GLS1,谷氨酰胺酶1;GLUL,谷氨酰胺合成酶;TGF-β,转化生长因子-β;IL,白细胞介素;TNF-α,肿瘤坏死因子-α。

    图  1  炎症反应中巨噬细胞代谢重编程流程图

    Figure  1.  Metabolic reprogramming flow chart of macrophages in inflammatory response

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出版历程
  • 收稿日期:  2025-04-25
  • 录用日期:  2025-06-10
  • 出版日期:  2025-12-25
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