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oai:repisalud.isciii.es:20.500.12105/156942024-09-27T08:31:00Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Hidalgo, Andres author Libby, Peter author Soehnlein, Oliver author Aramburu, Iker Valle author Papayannopoulos, Venizelos author Silvestre-Roig, Carlos author 2022-10-21 At the frontline of the host defence response, neutrophil antimicrobial functions have adapted to combat infections and injuries of different origins and magnitude. The release of web-like DNA structures named neutrophil extracellular traps (NETs) constitutes an important mechanism by which neutrophils prevent pathogen dissemination or deal with microorganisms of a bigger size. At the same time, nuclear and granule proteins with microbicidal activity bind to these DNA structures promoting the elimination of entrapped pathogens. However, these toxic properties may produce unwanted effects in the host, when neutrophils uncontrollably release NETs upon persistent inflammation. As a consequence, NET accumulation can produce vessel occlusion, tissue damage, and prolonged inflammation associated with the progression and exacerbation of multiple pathologic conditions. This review outlines recent advances in understanding the mechanisms of NET release and functions in sterile disease. We also discuss mechanisms of physiological regulation and the importance of neutrophil heterogeneity in NET formation and composition. Cardiovasc Res. 2022 Oct 21;118(13):2737-2753 10.1093/cvr/cvab329 1755-3245 Cardiovascular research 34648022 http://hdl.handle.net/20.500.12105/15694 Neutrophil extracellular traps: from physiology to pathology.