MINI REVIEW published: 07 August 2017 doi: 10.3389/fimmu.2017.00928 Neutrophil Extracellular Traps and Endothelial Dysfunction in Atherosclerosis and Thrombosis Haozhe Qi, Shuofei Yang*† and Lan Zhang*† Department of Vascular Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China Cardiovascular diseases are a leading cause of mortality and morbidity worldwide. Neutrophils are a component of the innate immune system which protect against patho- gen invasion; however, the contribution of neutrophils to cardiovascular disease has been underestimated, despite infiltration of leukocyte subsets being a known driving Edited by: force of atherosclerosis and thrombosis. In addition to their function as phagocytes, neu- Jixin Zhong, trophils can release their extracellular chromatin, nuclear protein, and serine proteases Case Western Reserve to form net-like fiber structures, termed neutrophil extracellular traps (NETs). NETs can University, United States entrap pathogens, induce endothelial activation, and trigger coagulation, and have been Reviewed by: Hugo Caire Castro-Faria-Neto, detected in atherosclerotic and thrombotic lesions in both humans and mice. Moreover, Oswaldo Cruz Foundation, Brazil NETs can induce endothelial dysfunction and trigger proinflammatory immune responses. Neha Dixit, DiscoveRx, United States Overall, current data indicate that NETs are not only present in plaques and thrombi but Shanzhong Gong, also have causative roles in triggering formation of atherosclerotic plaques and venous University of Texas at Austin, thrombi. This review is focused on published findings regarding NET-associated endo- United States thelial dysfunction during atherosclerosis, atherothrombosis, and venous thrombosis *Correspondence: Shuofei Yang pathogenesis. The NET structure is a novel discovery that will find its appropriate place
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