Fibrosis, a complex pathological process characterized by excessive deposition of extracellular matrix components, leads to tissue scarring and dysfunction. Emerging evidence suggests that neutrophil extracellular traps (NETs), composed of DNA, histones, and antimicrobial proteins, significantly contribute to fibrotic diseases pathogenesis. This review summarizes the process of NETs production, molecular mechanisms, and related diseases, and outlines the cellular and molecular mechanisms associated with fibrosis. Subsequently, this review comprehensively summarizes the current understanding of the intricate interplay between NETs and fibrosis across various organs, including the lung, liver, kidney, skin, and heart. The mechanisms by which NETs contribute to fibrogenesis, including their ability to promote inflammation, induce epithelial-mesenchymal transition (EMT), activate fibroblasts, deposit extracellular matrix (ECM) components, and trigger TLR4 signaling were explored. This review aimed to provide insights into the complex relationship between NETs and fibrosis via a comprehensive analysis of existing reports, offering novel perspectives for future research and therapeutic interventions.
Keywords: Epithelial-mesenchymal transition; Fibroblasts; Fibrosis; Mechanisms; Neutrophil extracellular traps.
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