Mechanisms of neutrophil extracellular trap in chronic inflammation of endothelium in atherosclerosis.

Cardiovascular diseases are a primary cause of morbidity and mortality around the world. In addition, atherosclerosis (AS)-caused cardiovascular disease is the primary cause of death in human diseases, and almost two billion people suffer from carotid AS worldwide. AS is caused by chronic inflammation of the arterial vessel and is initiated by dysfunction of vascular endothelial cells. Neutrophils protect against pathogen invasion because they function as a component of the innate immune system. However, the contribution of neutrophils to cardiovascular disease has not yet been clarified. Neutrophil extracellular traps (NETs) represent an immune defense mechanism that is different from direct pathogen phagocytosis. NETs are extracellular web-like structures activated by neutrophils, and they play important roles in promoting endothelial inflammation via direct or indirect pathways. NETs consist of DNA, histones, myeloperoxidase, matrix metalloproteinases, proteinase 3, etc. Most of the components of NETs have no direct toxic effect on endothelial cells, such as DNA, but they can damage endothelial cells indirectly. In addition, NETs play a critical role in the process of AS; therefore, it is important to clarify the mechanisms of NETs in AS because NETs are a new potential therapeutic target AS. This review summarizes the possible mechanisms of NETs in AS.