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However, the pathogenesis of myocarditis remains incompletely understood. Here, we report the presence of neutrophil extracellular traps (NETs) in cardiac tissue of patients and mice with myocarditis. Inhibition of NET formation in experimental autoimmune myocarditis (EAM) of mice substantially reduces inflammation in the acute phase of the disease. Targeting the cytokine midkine (MK), which mediates NET formation in vitro, not only attenuates NET formation in vivo and the infiltration of polymorphonuclear neutrophils (PMNs) but also reduces fibrosis and preserves systolic function during EAM. Low-density lipoprotein receptor\u2013related protein 1 (LRP1) acts as the functionally relevant receptor for MK-induced PMN recruitment as well as NET formation. In summary, NETosis substantially contributes to the pathogenesis of myocarditis and drives cardiac inflammation, probably via MK, which promotes PMN trafficking and NETosis. Thus, MK as well as NETs may represent novel therapeutic targets for the treatment of cardiac inflammation.<\/jats:p>","DOI":"10.1084\/jem.20181102","type":"journal-article","created":{"date-parts":[[2019,1,15]],"date-time":"2019-01-15T20:15:19Z","timestamp":1547583319000},"page":"350-368","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":124,"title":["Midkine drives cardiac inflammation by promoting neutrophil trafficking and NETosis in myocarditis"],"prefix":"10.1084","volume":"216","author":[{"given":"Ludwig T.","family":"Weckbach","sequence":"first","affiliation":[{"name":"Medizinische Klinik und Poliklinik I, Klinikum der Universit\u00e4t, Ludwig-Maximilians-University Munich, Munich, Germany 1"},{"name":"Walter Brendel Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-University Munich, Planegg-Martinsried, Germany 2"},{"name":"Institute of Cardiovascular Physiology and Pathophysiology, Biomedical 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