专职吞噬细胞胞葬功能在慢性创面修复中的作用机制及应用
The mechanism and application of specialized phagocytic cell burial function in chronic wound repair
蔺莉 1徐旭英1
作者信息
- 1. 首都医科大学附属北京中医医院,北京 100010
- 折叠
摘要
慢性创面作为一种长期消耗性疾病,是临床上长期难以解决的难题.胞葬作用功能障碍使创面凋亡细胞不能被及时清除,继而发生细胞坏死和促炎细胞因子释放,使创面难以由炎症期向增殖期过渡.巨噬细胞和树突状细胞作为专职的吞噬细胞,是胞葬作用的主要承担者,本文通过对两种专职吞噬细胞参与创面愈合过程的作用机理进行综述,发现除胞葬相关作用受体外,巨噬细胞和树突状细胞还分别通过作用于ICAM-1、NK-4,MIR-21、CD36等信号分子发挥胞葬作用,加速慢性创面的愈合.此外,树突状细胞的胞葬功能可能会受到SLC7A11的限制,去除或抑制SLC7A11可以显著增强树突状细胞的胞葬作用促进慢性创面愈合,本研究对进一步阐明慢性创面的愈合过程和创新治疗措施具有重要意义.
Abstract
Chronic wounds,as a long-term wasting disease,are a long-term clinical problem that is difficult to solve.Dysfunc-tion of efferocytosis prevents apoptotic cells from being cleared from the wound in time,resulting in secondary cell necrosis and re-lease of pro-inflammatory cytokines,making it difficult for the wound to transition from the inflammatory phase to the proliferative phase.Macrophages and dendritic cells,as professional phagocytes,are the main bearers of efferocytosis.This article reviews the mechanism of action of these two types of professional phagocytes in the wound healing process and finds that in addition to efferocytosis-related receptors,macrophages and dendritic cells also play a role in cytosis by acting on signaling molecules such as ICAM-1,NK-4,MIR-21,CD36,etc.,to accelerate the healing of chronic wounds.In addition,the efferocytosis function of den-dritic cells may be limited by SLC7A11.Removing or inhibiting SLC7A11 can significantly enhance the efferocytosis of dendritic cells and promote chronic wound healing.This study is of great significance to further elucidating the healing process of chronic re-fractory wound and the development of new treatmentss.
关键词
慢性难愈性创面/皮肤损伤/巨噬细胞/树突状细胞/胞葬作用/炎症消退Key words
Chronic refractory wounds/Skin damage/Macrophages/Dendritic cells/Cellular burial function/Inflammation subsides引用本文复制引用
基金项目
国家自然科学基金面上项目(82174388)
北京市百千万人才工程培养经费资助(2019A30)
第五批全国中医临床优秀人才(国中医药办人教函2021271号)
北京市医院管理中心"登峰"人才培养计划(DFL20220801)
出版年
2024
国家科技期刊平台
NSTL
万方数据