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

doi:10.3969/j.issn.1003-9198.2026.05.018

Abstract

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

CLC Number:

R 563

DANG Xiaoyu, ZHU Xiangyu, FAN Haoling, YAO Zitong, HUANG Jingjing. Research progress of macrophage senescence in immune microenvironment dysregulation of idiopathic pulmonary fibrosis[J]. Practical Geriatrics, 2026, 40(5): 525-529.

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

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