Abstract: Neutrophil extracellular traps (NETs) are complex structures released by neutrophils in response to inflammatory reactions,composed of DNA,histones,and various antimicrobial proteins,forming a web-like structure.While they defend against pathogen invasion,excessive accumulation can also lead to tissue damage and exacerbation of inflammation.In recent years,the pathological role of NETs in acute lung injury (ALI) has attracted widespread attention.The authors summarize the molecular mechanisms of NET formation in ALI,their pathological effects,and their potential as therapeutic targets.This article outlines the composition,structure,and formation process of NETs,revealing the DNA backbone in NETs and the binding pattern of histones and antimicrobial proteins,as well as the activation of peptidylarginine deiminase 4 (PAD4) in neutrophils that leads to the citrullination of histones,reducing their binding affinity to DNA and ultimately resulting in the formation and extrusion of NETs.This review analyzes the signaling pathways and regulatory mechanisms of NET formation,including the production of reactive oxygen species (ROS),chromatin decondensation,and the role of autophagy,which collectively promote the formation of NETs.Subsequently,this article discusses the pathological role of NETs in ALI,including their relationship with various stimuli,their impact on alveolar injury and inflammatory responses,and the destructive effects of NET components on alveolar epithelial and endothelial cells.Additionally,this review assesses the potential of NETs as therapeutic targets for ALI,including the possibility of NET components as diagnostic biomarkers and the detection methods for NET-related biomarkers in ALI.Lastly,the strategies of NETs in the treatment of ALI are explored,including pharmacological interventions and immunomodulatory methods,and their roles in regulating the formation and degradation of NETs,so as to provide a theoretical basis for the treatment of ALI and offer new directions for future research.

Key words: neutrophil extracellular traps; acute lung injury; molecular mechanisms; therapeutic strategies