The role of NETosis in enhancing of atherosclerosis.

Activated neutrophils release neutrophil extracellular traps (NETs), complex structures composed of extracellular genetic material and proteins sourced from the nucleus, granules, and cytoplasm in response to pathogenic inflammatory conditions. These NETs play a crucial role in the host's innate immune defense against invasive infections. Notably, in conditions like atherosclerosis, these extracellular formations can also be elicited by inflammatory stimuli such as lipids, prothrombotic factors, platelet aggregation, or proinflammatory cytokines.

Pathogenetic mechanisms of repeated adverse cardiovascular events development in patients with coronary heart disease: the role of chronic inflammation.

Stent restenosis is the most unfavorable complication of interventional treatment for coronary heart disease. We already know from various literature sources that the causes for stent restenosis in patients are both mechanical damage (partial opening, stent breakage, extended stented area, calcification, incomplete stent coverage of atherosclerotic plaque, weak radial stiffness of the stent metal frame, lack of stent drug coating), and the neointimal hyperplasia formation which is closely related to the de novo atherosclerosis development, being a predictor of the recurrent cardiovascular event.