Factor XII in inflammation and wound healingStavrou, Evi X.a,bCurrent Opinion in Hematology: September 2018 - Volume 25 - Issue 5 - p 403–409 doi: 10.1097/MOH.0000000000000450 HEMOSTASIS AND THROMBOSIS: Edited by Alvin H. Schmaier Abstract Author InformationAuthors Article MetricsMetrics Purpose of review This review describes the contribution of coagulation factor XII (FXII) in sterile inflammation and wound healing, focusing on recently identified roles for zymogen FXII in neutrophil functions. Recent findings Recent studies have identified an important role for FXII in neutrophil trafficking. In particular, following neutrophil activation, autocrine FXII signals through the urokinase plasminogen activator receptor (uPAR) on the neutrophil surface to upregulate neutrophil functions. The sum of these activities leads to neutrophil adhesion, chemotaxis, and neutrophil extracellular (NET) formation. Downregulating FXII-mediated signaling in neutrophils is associated with improved wound healing. Summary These recent findings show the sophisticated role of FXII in vivo and create new opportunities for research on the treatment of chronic inflammatory diseases. aDepartment of Medicine, Louis Stokes Veterans Administration Medical Center bDepartment of Medicine, Hematology and Oncology Division, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA Correspondence to Evi X. Stavrou, MD, Department of Medicine, Hematology and Oncology Division, Case Western Reserve University School of Medicine, 2143 WRB, 2103 Cornell Road, Cleveland, OH 44106, USA. Tel: +1 216 368 6986; fax: +1 216 368 1166; e-mail: email@example.com Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.