The mechanism and research progress of neutrophil extracellular traps on arteriosclerotic cardiovascular disease

doi:10.11958/20252054

Abstract

Abstract:

Atherosclerotic cardiovascular disease (ASCVD) is one of the leading causes of death worldwide, and its progression is closely related to the pathological effects of neutrophil extracellular traps (NETs). In atherosclerosis (AS), NETs aggravate the process of disease by promoting inflammatory response, inducing endothelial dysfunction, promoting thrombosis and other mechanisms. The components such as myeloperoxidase (MPO), neutrophil elastase (NE) and citrullinated histone H3 (CitH3) released by NETs can activate the immune inflammatory cascade, directly damage the vascular endothelium and promote thrombosis. In vascular inflammation, the formation of NETs is regulated by actin, and the released harmful molecules can induce endothelial cell apoptosis and drive the progress of inflammation through oxidative stress. The degradation and clearance of NETs depend on the action of enzymes such as deoxyribonuclease Ⅰ (DNase Ⅰ), and its regulatory mechanisms in atherosclerosis and vascular inflammation remain to be further studied. Based on the above mechanism, NETs-related markers have shown the potential as novel diagnostic and prognostic assessment biomarkers for ASCVD. This article aims to systematically elaborate the core pathological mechanism of NETs driving ASCVD through inflammatory activation, endothelial injury and thrombosis, providing a theoretical basis for targeted intervention.

Key words: atherosclerosis, cardiovascular diseases, extracellular traps, vascular inflammation

CLC Number:

R543.5，R323

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