实用老年医学 ›› 2026, Vol. 40 ›› Issue (5): 525-529.doi: 10.3969/j.issn.1003-9198.2026.05.018

• 讲座与综述 • 上一篇    下一篇

巨噬细胞衰老在特发性肺纤维化免疫微环境失衡中的研究进展

党小宇, 朱相瑜, 范浩玲, 姚子童, 黄菁菁   

  1. 211166 江苏省南京市,南京医科大学(党小宇,朱相瑜);
    210031 江苏省南京市,南京医科大学第四附属医院老年医学科(范浩玲,姚子童,黄菁菁)
  • 收稿日期:2025-10-18 发布日期:2026-05-20
  • 通讯作者: 黄菁菁,Email:jingjinghuang@njmu.edu.cn
  • 基金资助:
    江苏省老年健康科研项目(LKM2024023);江苏省干部保健科研课题立项项目(BJ24043);江苏省老年医学学会科研项目(JGS2025ZD004);南京市卫生科技发展项目(YKK24237)

Research progress of macrophage senescence in immune microenvironment dysregulation of idiopathic pulmonary fibrosis

DANG Xiaoyu, ZHU Xiangyu, FAN Haoling, YAO Zitong, HUANG Jingjing   

  1. Nanjing Medical University, Nanjing 211166, China(DANG Xiaoyu, ZHU Xiangyu);
    Department of Geriatrics, the Fourth Affiliated Hospital of Nanjing Medical University, Nanjing 210031, China (FAN Haoling, YAO Zitong, HUANG Jingjing)
  • Received:2025-10-18 Published:2026-05-20
  • Contact: HUANG Jingjing, Email: jingjinghuang@njmu.edu.cn

摘要: 本文旨在探讨巨噬细胞衰老在特发性肺纤维化(IPF)免疫微环境失衡中的核心作用,并对相关治疗前景进行展望。文章系统阐述了衰老巨噬细胞通过其独特的衰老相关分泌表型(SASP),打破免疫稳态,促进成纤维细胞活化和细胞外基质过度沉积,从而驱动IPF发生发展的关键机制。基于此,本文进一步评述了以清除衰老细胞、抑制SASP以及巨噬细胞重编程等为代表的治疗策略。最后指出,未来的研究应致力于解析巨噬细胞各亚群在疾病不同阶段的具体功能与转化轨迹,并提出治疗范式应向联合靶向策略转变,并推动个体化治疗在临床实践中的应用。

关键词: 特发性肺纤维化, 巨噬细胞, 细胞衰老

Abstract: This article aims to investigate the central role of macrophage senescence in the disruption of the immune microenvironment in idiopathic pulmonary fibrosis (IPF) and to explore related therapeutic prospects. It systematically elaborates on the key mechanism by which senescent macrophages, through their unique senescence-associated secretory phenotype (SASP), disrupt immune homeostasis, promote fibroblast activation, and drive excessive extracellular matrix deposition, thereby contributing to the pathogenesis and progression of IPF. Based on this, the article further reviews therapeutic strategies, including senolysis (targeted clearance of senescent cells), SASP inhibition, and macrophage reprogramming. Finally, it emphasizes that future research should focus on elucidating the specific functions and transformation trajectories of various macrophage subpopulations at different disease stages. A shift in therapeutic paradigms toward combined targeting strategies is proposed, along with advancing the application of personalized treatment in clinical practice.

Key words: idiopathic pulmonary fibrosis, macrophages, cellular senescence

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