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中华肾病研究电子杂志 ›› 2025, Vol. 14 ›› Issue (05) : 241 -247. doi: 10.3877/cma.j.issn.2095-3216.2025.05.001

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抑制急性肾损伤向慢性肾脏病转化:靶向致病性肾脏巨噬细胞纳米药物的应用
曾锐()   
  1. 430030 武汉,华中科技大学同济医学院附属同济医院肾内科、人畜共患传染病重症诊治全国重点实验室;器官移植教育部重点实验室、国家卫生健康委员会器官移植重点实验室、中国医学科学院器官移植重点实验室
  • 收稿日期:2024-10-31 出版日期:2025-10-28
  • 通信作者: 曾锐
  • 基金资助:
    国家自然科学基金(82370699)

Inhibition of the transition from AKI to CKD: application of nanomedicine targeting the pathogenic renal macrophages

Rui Zeng()   

  1. Department of Nephrology, Tongji Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology, State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory of Organ Transplantation of Ministry of Education, Key Laboratory of Organ Transplantation of National Health Commission, Key Laboratory of Organ Transplantation of Chinese Academy of Medical Sciences, Wuhan 430030, Hubei Province, China
  • Received:2024-10-31 Published:2025-10-28
  • Corresponding author: Rui Zeng
引用本文:

曾锐. 抑制急性肾损伤向慢性肾脏病转化:靶向致病性肾脏巨噬细胞纳米药物的应用[J/OL]. 中华肾病研究电子杂志, 2025, 14(05): 241-247.

Rui Zeng. Inhibition of the transition from AKI to CKD: application of nanomedicine targeting the pathogenic renal macrophages[J/OL]. Chinese Journal of Kidney Disease Investigation(Electronic Edition), 2025, 14(05): 241-247.

急性肾损伤(acute kidney injury,AKI)约20%~30%会发展为慢性肾脏病(chronic kidney disease,CKD)。AKI向CKD转化的机制主要涉及细胞损伤、氧化应激、线粒体功能障碍和免疫细胞异常活化。巨噬细胞作为AKI后浸润肾脏的主要免疫效应细胞,其表型具有高度异质性和可塑性,介导肾脏的损伤、炎症、修复和纤维化。鉴于广谱巨噬细胞的干预策略缺乏选择性,会破坏具有保护功能的巨噬细胞亚群,有必要开发靶向肾脏致病性巨噬细胞亚群的治疗药物。纳米药物凭借其可调控的理化特性、优异的生物相容性和生物屏障穿透能力,在靶向致病性巨噬细胞治疗肾脏疾病方面展现优势。本文主要介绍在AKI向CKD转化过程中巨噬细胞的表型变化和功能异质性、靶向肾脏巨噬细胞纳米药物的应用方法,以及肾小球滤过屏障对靶向肾脏巨噬细胞纳米药物滤过的影响。

Approximately 20 to 30 percent of patients with acute kidney injury (AKI) progress to chronic kidney disease (CKD). The mechanisms underlying this AKI-to-CKD transition mainly involve cellular damage, oxidative stress, mitochondrial dysfunction, and abnormal immune cell activation. Macrophages, as the primary immune effector cells infiltrating the kidney after AKI, exhibit high heterogeneity and plasticity in their phenotypes, mediating processes including renal injury, inflammation, repair, and fibrosis. Given the lack of specificity in broad-spectrum macrophage intervention strategies, which may disrupt protective macrophage subpopulations, it is imperative to develop therapeutic agents targeting pathogenic macrophage subsets in the kidney. Nanomedicines demonstrate advantages in treating kidney diseases by targeting pathogenic macrophages, leveraging their tunable physicochemical properties, superior biocompatibility, and biological barrier penetration capabilities. This article primarily introduced the phenotypic changes and functional heterogeneity of macrophages during the transition from AKI to CKD, the application methods of nanomedicines targeting renal macrophages, and the impact of the glomerular filtration barrier on the filtration of nanomedicines targeting renal macrophages.

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