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从NLRP3炎性小体视角看肺纤维化：作用机制与潜在治疗新进展

Pulmonary fibrosis through the prism of NLRP3 inflammasome: mechanistic pathways and prospective therapeutic innovations.

作者信息

Wang Mengxue, Xie Yuanyuan, Cao Yuqing, Yu Bing, Dai Qingqing

机构信息

Department of Critical Care Medicine, The Obstetrics & Gynecology Hospital of Fudan University, Shanghai, China.

Department of Critical Care Medicine, The Obstetrics & Gynecology Hospital of Fudan University, Yangtze River Delta Integration Demonstration Zone (QingPu), Shanghai, China.

出版信息

Front Immunol. 2025 May 5;16:1593729. doi: 10.3389/fimmu.2025.1593729. eCollection 2025.

DOI:10.3389/fimmu.2025.1593729
PMID:40391214
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12086142/
Abstract

Pulmonary fibrosis is a disease that severely affects the patients' life quality, characterized by lung tissue remodeling and functional impairment. Recent research has found that the NLRP3 inflammasome plays an important role in the pathogenesis of pulmonary fibrosis. Although existing researches have revealed the potential role of NLRP3 in pulmonary fibrosis, many mysteries still remain regarding its specific mechanisms and clinical applications. This article aims to review the mechanisms of action of NLRP3 in pulmonary fibrosis, related signaling pathways, and the latest research progress on its potential as a therapeutic target, in hopes of providing new ideas and directions for future clinical treatment.

摘要

肺纤维化是一种严重影响患者生活质量的疾病，其特征为肺组织重塑和功能损害。最近的研究发现，NLRP3炎性小体在肺纤维化的发病机制中起重要作用。尽管现有研究已经揭示了NLRP3在肺纤维化中的潜在作用，但其具体机制和临床应用仍存在许多谜团。本文旨在综述NLRP3在肺纤维化中的作用机制、相关信号通路及其作为治疗靶点的最新研究进展，以期为未来的临床治疗提供新的思路和方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45b3/12086142/cce59023df9b/fimmu-16-1593729-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45b3/12086142/cce59023df9b/fimmu-16-1593729-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/45b3/12086142/cce59023df9b/fimmu-16-1593729-g001.jpg

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Pulmonary fibrosis through the prism of NLRP3 inflammasome: mechanistic pathways and prospective therapeutic innovations.

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本文引用的文献

[1]
Unraveling the priming phase of NLRP3 inflammasome activation: Molecular insights and clinical relevance.

Int Immunopharmacol. 2025-1-27

[2]
Endoplasmic reticulum stress in acute lung injury and pulmonary fibrosis.

FASEB J. 2024-12-15

[3]
The application and prospects of drug delivery systems in idiopathic pulmonary fibrosis.

Biomater Adv. 2025-3

[4]
GLP-1R activation attenuates the progression of pulmonary fibrosis via disrupting NLRP3 inflammasome/PFKFB3-driven glycolysis interaction and histone lactylation.

J Transl Med. 2024-10-21

[5]
Enhanced oxidative stress aggravates BLM-induced pulmonary fibrosis by promoting cellular senescence through enhancing NLRP3 activation.

Life Sci. 2024-12-1

[6]
Idiopathic Pulmonary Fibrosis Caused by Damaged Mitochondria and Imbalanced Protein Homeostasis in Alveolar Epithelial Type II Cell.

Adv Biol (Weinh). 2025-4

[7]
GAMG ameliorates silica-induced pulmonary inflammation and fibrosis via the regulation of EMT and NLRP3/TGF-β1/Smad signaling pathway.

Ecotoxicol Environ Saf. 2024-10-15

[8]
Cellular and Molecular Genetic Mechanisms of Lung Fibrosis Development and the Role of Vitamin D: A Review.

Int J Mol Sci. 2024-8-16

[9]
NLRP3 inflammasome activation contributes to the development of the pro-fibrotic phenotype of lung fibroblasts.

Biochem Pharmacol. 2024-11

[10]
Construction of the pulmonary bio-adhesive delivery system of nintedanib nanocrystalline for effective treatment of pulmonary fibrosis.

Int J Pharm. 2024-7-20

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