巨噬细胞极化在肾缺血再灌注损伤中的研究进展
作者:
作者单位:

1.河南中医药大学第一附属医院泌尿外科,郑州 450003;2.河南中医药大学第一临床医学院,郑州 450003

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R-33


Research developments in macrophage polarization in renal ischemia-reperfusion injury
Author:
Affiliation:

1. Department of Urology, the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450003, China. 2. the First Clinical Medical College of Henan University of Chinese Medicine, Zhengzhou 450003

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    摘要:

    巨噬细胞是先天免疫中重要的免疫细胞,具有显著的异质性和极化性。在微环境中各种因子的刺激下可极化为各种表型(主要是M1和M2),从而发挥不同的作用和功能,在肾缺血再灌注损伤(renal ischemia-reperfusion injury,RIRI)的病理生理机制中发挥重要作用。过度的免疫反应必然会导致组织损伤,M1型巨噬细胞是促炎细胞,参与病原体的清除;而M2型巨噬细胞具有抗炎作用,参与RIRI后肾组织修复和重塑。巨噬细胞表型之间的平衡对于RIRI的结局和治疗十分重要。故本文从巨噬细胞极化角度切入,对巨噬细胞在RIRI中的病理生理机制和最新的治疗方案进行阐述,旨在为进一步研究巨噬细胞极化在RIRI中的作用提供参考,为通过调节巨噬细胞极化来改善RIRI的治疗策略提供思路。

    Abstract:

    Macrophages are important immune cells involved in innate immunity, with significant heterogeneity and polarization. Macrophages can polarize into different phenotypes (mainly M1 and M2) under stimulation by various factors in the microenvironment, leading to different roles and functions. Macrophages play an important role in the pathophysiological mechanism of renal ischemia-reperfusion injury (RIRI). An excessive immune response will inevitably lead to tissue damage. M1 macrophages are pro-inflammatory cells involved in the clearance of pathogens, while M2-type macrophages have anti-inflammatory effects and participate in the repair and remodeling of renal tissue after RIRI. The balance between these macrophage phenotypes is thus an important factor affecting the outcome and treatment of RIRI. This review considers the pathophysiologic mechanism of macrophages in RIRI and the latest treatments from the perspective of macrophage polarization, with the aim of supporting further studies of the function of macrophage polarization in RIRI and adjusting the macrophage polarization process to improve RIRI treatment strategies.

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孙豪杰,刘宪勤,王锁刚.巨噬细胞极化在肾缺血再灌注损伤中的研究进展[J].中国比较医学杂志,2025,35(1):172~180.

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  • 收稿日期:2024-06-16
  • 在线发布日期: 2025-04-18