Increased Neutrophil Extracellular Traps Related to Smoking Intensity and Subclinical Atherosclerosis in Patients with Type 2 Diabetes
Michael Koutsilieris, Petros P. Sfikakis, Antonios Chatzigeorgiou, Ioannis Mitroulis, Akrivi Chrysanthopoulou, Aigli‐Ioanna Legaki, Konstantinos Ritis, Nikolaοs Tentolouris, Athanase D. Protogerou
Abstract
Atherosclerosis is a complex chronic inflammatory process of medium to large-sized arterial vessels, which leads to cardiovascular diseases (CVDs), including coronary artery disease and cerebrovascular disease. Endothelial cell dysfunction and activation, leading to infiltration and accumulation of inflammatory leukocytes in the subendothelial space, are key steps in the generation of atherosclerotic plaques.[1] Beyond endothelial cells and platelets, neutrophils have recently emerged as important players in the development of atherosclerosis, through the release of neutrophil extracellular traps (NETs),[2] which are extracellular structures composed of DNA and neutrophil peptides.[3] Studies in the Apoe −/− mouse model suggest that neutrophils contribute to atherogenesis, via the release of NETs.[4] However, studies in human plaque samples suggest that neutrophils and NETs are present only in unstable plaques and upon plaque rupture,[2] [5] being the main leukocyte population present in thrombi at the atherothrombotic sites.[6] [7]